How Zombie Cells Speed Up Aging

As we saw last week, aging is a process by which your body speeds up or slows down depending on how poorly or well it functions. From a cellular standpoint, we saw that cellular senescence (the aging and dysfunctioning of human cells) can lead to a number of diseases, all of which look and smell like “aging”. From an even deeper level, we saw that mitochondrial dysfunction (mitochondria being the powerhouse of the human cell) causes a human cell to lose its power potential, thereby also causing a number of side-effects and potential diseases, all of which walk and talk like “aging”.

Hopefully, you’re starting to put the picture together that the societal idea of “aging” as we get older is false. Do we still age to some degree as we get older? Yes. Do we still have an increased risk of developing chronic disease as we get older? Sure. However, if you build a lifestyle that supports your bodily function instead of works against it, your chances of aging poorly and developing chronic disease decrease…significantly.

Now, before we jump into environmental and behavioral causes of mitochondrial dysfunction or cellular senescence, we have one more connection to make to bring our aging picture full circle…

The Attack of the Killer Zombie Cells…

When a cell becomes zombie-like, its mitochondria become dysfunctional. When mitochondria become dysfunctional, especially in zombie cells, they are unable to produce enough antioxidants to balance out and kill the free radicals it’s also producing. Excess free radicals lead to chronic inflammation, which leads to, you guessed it, symptoms of aging such as arthritis, wrinkles, macular degeneration, and more.

Now, the question is, what is the cell SUPPOSED to instead? If we don’t want it to become zombie-like, then what do we want it to do?

Like all of life, a cell has a natural life cycle, it lives, and then it dies. Which is exactly what a cell should do. A healthy cell can die in one of 2 ways: The first process of cell death is called apoptosis, which, in Ancient Greek, literally means “falling off”. So, these dying cells are falling off, or, more directly, committing suicide, in a natural, programmed way.

On the other hand, a cell can die through a process called autophagy, again in Ancient Greek literally meaning “self-devouring”. So, the cell devours itself internally instead of “falling off” and shrinking into cellular suicide. Of course, these processes seem very similar from a high level, but they require very different chemicals and proteins in order to execute at the cellular level.

Nonetheless, both apoptosis and autophagy are how a human cell should die without disrupting the cells around it or causing long-term harm to your body. Of course, this is only able to happen if the cell is functioning properly, which means that its mitochondria are up and running, and it is not in a zombie-like state, as it would be with cellular senescence.

So, what causes mitochondria to become dysfunctional or a cell to become a zombie? Well, there are 2 underlying factors. And, as the Ancient Stoic philosophers would say, one factor we have no control over, and the other factor we have some, but not complete control over…

Genetics VS Epigenetics…Which One Counts More?

In other words, if you’re born with a certain gene or genes, the belief is that you are destined to develop whatever that gene or genes have in store for you. Let’s use an example…

One chronic disease that is especially scary is Alzheimer’s. From a genetic standpoint, there are 3 genes that are closely associated with Alzheimer’s disease: APOe2, APOe3, and APOe4. You inherit one APO gene from your mom and one from your dad, so there are a total of 6 potential APO “combinations” you have yourself: e2/e2, e2/e3, e3/e3, e3/e4, e4/ e4.

Research shows that the more high numbers you have as APO combinations, the higher your likelihood of developing Alzheimer’s. In other words, if you have 2 APOe2 genes, you have a small and insignificant chance of developing the disease while having 2 APOe4 genes means you have a high and potentially significant likelihood of developing Alzheimer’s.

Years ago, if you were tested and were found to have 2 APOe4 genes, your doctor would’ve prepared you for the worst and convinced you that you’re going to develop Alzheimer’s at some point in your life whether you like it or not. That type of thinking is guided by the “genetic” theory of aging. We are and become what our genes are coded to become.

However, recent research is slowly starting to debunk this type of thinking. As a matter of fact, research on another type of genetics is showing that your genetic code actually has less to do with how you age then previously thought.

The other type of genetics I’m talking about is called epigenetics. The prefix, epi, comes from Ancient Greek and means “over, outside of, or around”.  Epigenetics is the changes in the “expression” of a gene (how a gene releases the information it carries) without changing the underlying DNA sequence of the gene itself. In other words, while genetics are changed and developed over generations and generations, epigenetics is changed and developed from one generation to the next and within the current body that’s developing…which is YOU.

There are many factors that impact your epigenetics. However, the factors that are most obvious and easiest to understand include the environment you live in, the behaviors you take a part in, and the mindset and mentality you build as you participate in life.

Now, to bring this back to how we started this essay, cellular senescence and mitochondrial dysfunction play a big role in how we age. Both of these cellular issues are epigenetic factors. Cellular senescence, being a natural program of life, is either increased or decreased based on your environment, how you behave, and how you think. The same exact rules apply to mitochondrial dysfunction. It is epigenetic in nature, meaning it has the potential to negatively or positively impact gene expression based on your environment, your behavior, and how you think.

So, now that we’ve covered some of the most important hallmarks of aging in our previous essay, cellular senescence, and mitochondrial dysfunction, and learned more specifically how senescent cells AKA zombie cells impact how you age, also through mitochondrial dysfunction, AND how these epigenetic factors play a bigger part in our development than our genes do, NEXT TIME we’ll take a look at how we start to turn around these epigenetic factors to allow our genetic code work FOR us instead of AGAINST as we strive to age so that we can participate in the Centenarian Olympics on our 100th birthday.