Playing This Chess Game Called Life

A lot of it boils down to understanding how the sequence of events plays out.

The game of chess is a 2-player strategic board game that can last for hours. Each player has 16 pieces to control and move, and there are so many different permutations and combinations to move those pieces that it can be absolutely mind blowing.

The players who know how to play have many different variations of opening their offensive or defensive strategies that it would be impossible to cope with the memorisation of that sheer lot of them. In moving the pieces, too, we see a common theme approaching — it is a sequential process.

One has to make a coordinated, sequential and strategic effort to checkmate the other side; or if one is on the losing end, at least make the most out of it and force the game into a draw. A series of blunders and missteps throughout the game can easily turn the game around, even for players at grandmaster level. Contingency planning and a lot of “what-ifs” are key here — considering all angles helps them to see the big picture more clearly. That is why some players are also willing to sacrifice high value pieces to be able to get to the final checkmate point — though we have to admit sometimes that they can be blundering moves (oops!).

A chess player has to consider these sequential processes and look at pre-empting moves that could be made 20 or 30 steps later in their overall strategy. The sequence of events is extremely important. Knowledge is key here — what can trigger a cascade of inopportune events that can lead to a checkmate?

Why Is This So Important?

Why I bring this up is that many of us go through life without planning for or considering the sequence of events that can cascade throughout our life. As Benjamin Franklin aptly described it, “If you fail to plan, you are planning to fail!”

Granted, it is impossible to know everything — unexpected events can occur, for instance. We may not have any ability to predict those. For example, the COVID-19 coronavirus pandemic sweeping the whole world and obliterating a ton of jobs could not be expected — the people working those jobs in December would have been under the impression that their jobs were safe then — but the sequence of events caused by one virus ended up with them losing their jobs.

But what about the events that can be expected and that can be pre-emptively averted?

Again, Knowledge is Power

We do need to know what we can control and what we can’t. We can’t control how the virus spreads, and how it affects the economy. But we can control how we operate, and how we can take measures to reduce the risk of getting infected by the virus, for instance.

How does an infection occur, and why do some people suffer severe effects of the infection while others don’t?

Virus infection is a sequential process. The virus spreads via airborne droplets, which does mean that wearing masks to add an additional protective layer against the breathing in of droplets containing the infectious virus can reduce the risk of contracting an infection. It doesn’t guarantee that we will be safe from it completely, but we can reduce the risk involved.

Knowing that we have antibodies is one thing, but they aren’t the only thing. Antibodies are proteins that function as tags — they tag viruses and infected cells within our body. Cells that are infected with viruses are literally undergoing hypnosis — these cells are doing the bidding of the virus and are very much being virus photocopiers. They will be producing more copies of the virus that can then proceed to infect other healthy cells. Their virus replication mechanism has to be halted, and they have to be destroyed to prevent further copies of the virus being produced.

For example, if a supermarket has a vermin problem, and the vermin are eating away at the food products in the supermarket, the pest control team has to come in and eradicate all the vermin. This prevents further damage to the products.

But does the pest control team remove the damaged food products?

No, it doesn’t. The supermarket staff will either have to engage a waste disposal team at their own cost, or they would themselves have to dispose of the damaged products. The products aren’t going to be removed on their own volition.

In the same way, the body has to dispose of all these tagged infected cells.

These tagged cells are attacked by the immune system, where they are programmed to commit suicide via apoptosis. The dead cells can then be digested by phagocytes in a process known as phagocytosis, which are in essence scavenger cells that devour the dead cells, such that whatever DNA/RNA material in there can be decomposed right down to its constituent nucleic acids, which can then be used as building blocks to synthesise new DNA molecules for new cells.

That’s also how autophagy works in our body for a renewal of our body’s cells — when a healthy cell has outlived its usefulness, it will be tagged by the p62 protein (not the same as an antibody), and the phagocytes will come and digest them up for DNA/RNA material reuse through phagocytosis.

Hence, we see a sequential process forming. Firstly, an infected cell must be tagged. Secondly, the tagged cell must be destroyed and its contents recycled.

What happens when we do contract an infection, then?

It means that either our antibody tagging rate is slow, or the phagocytosis function is slow. The process is only as fast as the slowest process, or as Thomas Reid once said, “A chain is only as strong as its weakest link.”

Because what good is it for an antibody to be able to tag 500 infected cells in an hour, for instance, while phagocytosis can only eliminate 50 cells per hour?

It means that the overall rate of elimination is only 50 cells per hour. We are only as strong as our weakest link. Also, an apoptotic cell that does not get cleared off quickly enough will end up releasing pro-inflammatory signals into the blood, much like how a dead body gives off foul odours and decomposes into an unsightly mess if it is not quickly buried, cremated, or weighed down and thrown into the sea.

Unfortunately, medical research these days is focusing on the development of antibodies and drugs for preventing virus replication, while nobody really talks about phagocytosis or autophagy, surprisingly (one can do a cursory search on the Medium Coronavirus Blog to see how many articles discuss antibodies and drugs, as compared to how many articles even discuss phagocytosis).

But why would this sequence be important in the first place?

A compromised autophagy process would result in the accumulation of all these virus-infected cells. It is mentioned in this article that people with a dysfunctional autophagy process include those with Type 2 diabetes, cancer, heart disease and neurodegenerative diseases.

Unfortunately, these health situations are also chronic inflammatory conditions, which manifest as a result of a dysfunctional pro-inflammatory signal coming out of the nuclear factor kappa B (NF-κB) transcriptional pathway. A dysregulated NF-κB pathway tends to produce more pro-inflammatory cytokines than normal, such as interleukin-1 beta (IL-1β).

What can excessive IL-1β do?

1. It can signal cells to disregard the insulin signal for glucose uptake, resulting in the development of insulin resistance and ultimately Type 2 diabetes, as I explain in Type 2 Diabetes — A Case of The Immune System Gone Bad, Too?
2. It signals osteoclast (cells that dissolve bone mineral) activity to increase. When osteoclast activity increases, bone mineral dissolves more rapidly, which can then lead into osteopenia and osteoporosis — for a more comprehensive coverage, do check out Why Does Osteoporosis Affect Post-Menopausal Women More Significantly Than Other People?
3. It signals our immune system’s macrophage cells to produce more matrix metalloproteinase (MMP) enzymes, which digest collagen. More MMPs mean a faster collagen digestion rate, which would affect not only our joint structure, leading to osteoarthritis (What The Deuce Is Different Between Osteoarthritis and Rheumatoid Arthritis?) and heart attacks or strokes (Now Seriously, What’s So Tricky About Cholesterol?)

So not only can an overproduction of IL-1β do all that… But this article and this article also do show how IL-1β can contribute to the development of lung damage and pulmonary fibrosis, which we know to be more likely to occur in patients with dysregulated autophagy mechanisms. And of course, the dreaded cytokine storm can develop. Especially when IL-1β also triggers a highly pro-inflammatory cell death via pyroptosis.

It becomes a more understandable sequential process now, doesn’t it?

Would it also explain why “relatively healthy” individuals can also be at risk of lung damage? Yes, because they may be “relatively healthy” while already experiencing a “dysregulated autophagy”, which is not exactly a medical condition on its own — there isn’t any real method available to quantify how well our autophagy process is working within. As a result, nobody ever talks about it or even considers it important in the grand scheme of things.

Unfortunately, this sequence cannot be rectified instantaneously.

Autophagy dysregulation doesn’t occur overnight. It is a “little by little” process. As I explained in my weight loss article (What I Learnt From A One Year Weight Loss Experiment), consistency is key.

We may not be doing something that is “consistently” good, but we may be indulging in other habits that are “consistently” bad. For example, in sleeping odd hours, we are depriving ourselves of quality sleep, which, if done consistently, is one of the lifestyle patterns that can affect NF-κB in a sequential process, as I explain in Four Ways That Our Lifestyle Affects Our Immune System.

It’s the little things that matter. Much like in a chess game, where every move has to be made with much consideration and strategy involved (and that’s why some chess games can last for hours!), there is a need in understanding the sequential process of what goes on in our bodies, so that we can better equip ourselves with the knowledge of how to pre-empt and prevent certain risks from occurring (or simply by reducing the probability of the risk significantly).

And that’s life!

It is a cascade of sequential processes. One thing leads to another. We can’t simply isolate an event and decide that it is the only factor that contributes to the problem.

There are multiple other angles and perspectives to consider. Just by considering this scenario on health alone, there are so many factors that contribute to how our bodies respond to a viral infection.

But in your decision making — what do you know, and what don’t you know?

That’s a very important concept to get, because knowing more allows one to be more prepared and to strategise for contingencies should the need ever arise!

Joel Yong, PhD, is a biochemical engineer/scientist, an educator and a writer. He has authored 1 ebook (which is available on Amazon.com in Kindle format) and co-authored 6 journal articles in internationally peer-reviewed scientific journals. His main focus is on finding out the fundamentals of biochemical mechanisms in the body that the doctors don’t educate the lay people about, and will then proceed to deconstruct them for your understanding — as an educator should. Do visit his website here to connect.