The causes of aging are varied and multi-faceted, but one specific target that has captured the attention of researchers for a while now is your cell’s powerhouse – also known as the mitochondria. More and more evidence shows a relationship between changes in the functioning of your mitochondria and the aging process. In fact, there may be an even bigger link here than we previously thought.
Specifically, there are three elements of mitochondrial biology that are of interest to the question of how and why we age.
These elements include:
- The way in which the mitochondria may regulate our immune system
- The role of mitochondrial quality and health in developing age dependent diseases
- The way that mitochondria send signals to the body as a whole that could affect the rate at which we age.
Before we get too deep here though, what exactly are mitochondria and what do they do? It’s a great question and it’s a topic that can get a little complex – but it’s definitely worth learning some answers here.
Mitochondria, which is almost always referred to as the “powerhouse” of the human cell, is responsible for creating energy from the food we eat. They also create the majority of our ATP (adenosine triphosphate) – our energy “currency”. And finally, they’re involved in a big way in cell signaling and cell death or “apoptosis”.
So, what are some of the causes of aging related to mitochondria?
Here are a few ideas, based on the current scientific research:
Mitochondria and the Inflammation of Aging
One thing that researchers are starting to realize about aging is that it’s associated with evidence of an over activation of our immune system. This can ultimately lead to what’s know as “inflammaging”. A good example where this can be seen is in older individuals, where those who are in worse physical health have higher levels inflammation in their body.
Things that you may or may not have heard of like C-reactive protein, IL-6, and fibrinogen are all inflammatory compounds within your body and are found more consistently in these people than in their healthier peers.
And when you look a little deeper, an analysis of the levels of these compounds is pretty telling: elevated IL-6 levels in the blood for example, are actually directly correlated with a higher rate of disability, frailty, slower walking speed, and overall mortality.
Another group of powerful compounds in the body that increase inflammation are known as inflammatory cytokines. Like other things that cause inflammation, these are also often higher in older individuals who are already in poor health, and are found to be lower often times in people that have healthy immune systems and aren’t actively fighting a disease (those actively fighting a disease or sickness can see an increase in inflammatory cytokines).
Inflammatory cytokines can amp up the body’s defenses when you’re sick – and actually get your body healthy with inflammation.
But when they run rampant and get out of control in creating that same inflammation – that’s when you have a problem.
Keep in mind that inflammation in general is actually a natural process in the body which is entirely necessary for our survival and can at times be incredibly beneficial. But pro-inflammatory processes whereby the body gets focused too much on creating inflammation (as with the overactive inflammatory cytokines) become detrimental to your health.
In fact Artherosclerosis, Alzheimer’s disease, and metabolic syndrome (pre diabetes) all are now known to have overly high levels of inflammation as a contributing cause.
So how is the mitochondria involved in the inflammation that causes aging? There are a few ideas on this, one being the “danger theory” argument. And, despite it’s funny name, it seems to make sense.
The danger theory rests on the idea that the immune system is capable of being aware of – and responding to – tissue damage. This can be good, but one of the potential downsides here is that when the immune system responds to that damage, it sometimes views some of the molecules that are released as a result the same way as it would view dangerous pathogens.
And hence it responds accordingly. This immune response that is then triggered is often termed damage-associated molecular patterns (DAMPs).
The idea here, unfortunately, is that the mitochondria which have developed over billions of years to be involved in our immune response now go into overdrive, spitting out various forms of these DAMPs, which then start slowly increase inflammation and age related deficits.
There are myriad other ways that mitochondria interact and are interacted with the immune system, but the danger theory starts to give you an idea of one of the more important potential causes of aging when it comes to mitochondria.
Mitochondrial DNA and Aging
One of the other issues with mitochondria as it relates to aging is the damage that can occur to mitochondria itself over time.
As you age, your mitochondria naturally experience a greater level of mutations in response to different stressors. The question is does the mitochondria age because you age, or do you age because your mitochondria get older and experience more mutations? Researchers may not have the full answer here.
It has been found, however, that over 300 mutations exist in human mitochondrial DNA, and these mutations are linked to a number of wide conditions, including Parkinson’s disease and other age-related disease states. Another example of damaged DNA causing aging is found in people with HIV infection.
These individuals typically exhibit aspects of accelerated aging including frailty, increased risk and rate of cardiovascular disease, and a much higher risk of bone fractures.
Mitophagy and Aging
As people get older, they often experience something called sarcopenia, which is an age related loss of muscle mass and strength. It appears that working out as you age can help protect against this, but it also appears that some of it may not be preventable and that it’s directly linked to your mitochondrial function.
Research now shows that as you age, the mitochondria in your muscles produce less ATP (one of their main jobs) and have a reduction in their respiratory capacity by almost 50%. These deficits seem to track closely with a decrease in muscular strength and are believed to be linked to the development of sarcopenia mentioned above.
As a trainer, the question I have is to what extent can you prevent muscular decline (both the decrease in strength and muscle mass) by keeping the mitochondria healthy? And – once you start to keep the mitochondria healthy – what affect does that have on your aging process and physical capacity down the line?
We do know though that keeping your mitochondria healthy may not be the easiest thing to do though (even though we have a lot of ideas on how to do it), and age is a tough rival. (Stay tuned for another post soon where I talk about some of the current scientifically backed ways to keep your mitochondria healthy).
A few of the things that age seems to cause that affect the mitochondria that then directly impact things like strength and muscle mass are: accumulation of mutations within the mitochondria, age dependent damage to non-mutated mitochondria, and a decline in the removal of dysfunctional mitochondria from the same cause.
The current thought is that it’s likely some combination of these causes that interact to create your mitochondrial break down.
And this is where something called mitophagy comes in. Mitophagy is the process whereby cells in your body selectively destroy themselves and the idea is that older or defective cells are often the ones that get destroyed. This is a normal process, and can be really good.
In fact, when mitophagy is high IE the body is destroying a lot of the older or damaged mitochondria, the over activation of the immune system (that could spark disease) also stays low.
The way mitophagy works on a micro level isn’t something researchers have figured out completely, but we do know that mitophagy markedly declines in many mammals as they age.
A related problem that’s seen (as is part of the aging process) is the rise in reactive oxygen species (ROS), AKA free radicals as mitophagy decreases. Mitophagy and a similar process known as autophagy help reduce the overabundance of these compounds in the body, and this is part of the reason antioxidant rich foods or antioxidant supplements may be helpful in slowing aging.
Oxidative stress is linked to aging and when mitochondria are healthy they help to tamp down the free radicals that contribute to this. And again, there are studies that show antioxidants may help “clean up” the oxidative stress when damaged (or even nonexistent in the case of animals in studies bred to lack efficient autophagy) mitochondria can’t do that job.
On the other hand, there is evidence showing when ROS (or the free radicals for the sake of simplicity) are allowed to run rampant, some species of animals actually live longer. So the jury is not fully out yet, but we do know that we probably need a balance of both experiencing some oxidative stress and not as much – so antioxidants may definitely still be useful – especially considering how abundant they are in so many plant compounds we consume.
Further interesting research has shown that when the amount of autophagy or mitophagy is artificially increased or enhanced in certain animals, they tend to live longer. This is sometimes done by genetically manipulating the animals from the start, but it’s also done with certain compounds and with certain imposed restrictions like fasting, which seems to improve the health of mitochondria.