We All Have Zombie Cells! Here’s What I Mean

Zombie cells! They are real, they are scary and they make you age! In medical parlance, these are called senescent cells. These are aged cells that no longer replicate, but also don’t die. The process by which cells become zombies is called cellular senescence, and is probably the scariest hallmark of ageing.

What is cellular senescence?

Our cells are constantly replicating, but after about 50 replications cells begin to break down and lose function. Every time a cell divides, it ages, and this process is accelerated by stress-inducing factors (like DNA damage, oxidative damage, abnormal cell growth and the activation of genes that could promote cancer growth).?

As we discussed under telomere alteration, telomeres at the ends of DNA structures protect it from damage. As our cells continue to divide, a part of the telomere is lost each time. With time, it gets shorter and shorter, ultimately leaving the? DNA unprotected. At this stage, the cell stops replicating. Even though our body has damage repair mechanisms for our cells, they aren’t always able to fix the damage. This leads to one of two things:

• the cell is destroyed?
• the cell stays alive and becomes a senescent cell, like a zombie!

Senescent cells - like zombies - look different from normal cells and are not easy to kill. Although these cells aren’t able to replicate, they remain active on some level. They no longer support the tissues of which they are part of, instead they emit a range of potentially harmful chemical signals that encourage nearby healthy cells to enter the same senescent state. And as these zombie cells build up in our body, they also prevent new cells from being made.

Senescent cells have been strongly associated with multiple problems:?

• Reduce tissue repair
• Increase chronic inflammation
• Cancer?
• Type 2 diabetics?
• Other age-related disorders

Senescence-associated secretory phenotype (SASP):

SASP is a phenotype associated with senescent cells. Those cells secrete high levels of inflammatory cytokines, immune modulators, growth factors, and proteases. SASP may also consist of enzymes, microRNA, DNA fragments, chemokines, and other bioactive factors. Initially, SASP is immunosuppressive and profibrotic (fibrosis is the thickening and scarring of connective tissue) , but progresses to become proinflammatory and fibrolytic. SASP is considered to be the primary cause of the detrimental effects of senescent cells.

Cellular Cannibalism:?

A study found that cells that had become scenecent after treatment with chemotherapy actually ate their neighbouring cells alive. This is called cellular cannibalism: one cell entirely engulfs another cell. After eating their healthy neighbours, senescent cells tend to survive much longer than non-cannibal cells.

However, unlike zombies, senescent cells aren’t completely useless. They play a role in tissue and wound repair and are surprisingly also associated with protection against cancer.?

This dual situation can be explained by something called Antagonistic Pleiotropy - the ability for traits to be beneficial during youth but detrimental during old age. Senescent cells may be very useful for healing wounds and preventing cancer in our youth. But as they accumulate, we get all the negatives discussed earlier.?

So what now? Do we live with them or can we do something about this?

Work is being done on creating drugs that will clear senescent cells from our body without disturbing healthy cells. Senescent cell destroying drugs, senolytics, are in the development process.?

In the meantime, you can increase the consumption of:?

i. Quercetin: onions, kale, cherry tomatoes, broccoli, blueberries & apples

ii. Fisetin: nuts, wine, cucumber, onions, tomatoes, grapes, kiwis, persimmons, mangoes, apples & strawberries?

iii. Piperlongumine (long pepper)

Their consumption has been shown to clear senescent cells in the body.

Intermittent fasting is known to trigger autophagy and get rid of the dysfunctional units in your cells. However, the studies so far have shown conflicting results and we will be discussing this in a later edition, where I will deep dive into autophagy. Stay tuned.

This newsletter is a part of our ongoing series The Longevity Hack. Our aim is to help you understand the science, learn to recognise the markers of ageing and to develop biohacks for each of these. Next week, we will look at stem cell exhaustion. You can read the previous editions here.?

Curious to know more about longevity, ageing and how you can cultivate a lifestyle which will help you live longer, healthier and happier???

Drop me a message on LinkedIn or Instagram to set up a 1-on-1 conversation.?

See you next week!