Mitochondria and Aging

Posted on May 15, 2019 at 4:00 PM

Mitochondria and Aging

Mitochondria produce energy and release free radicals in the process. Free radicals are unstable molecules that can damage the cells in your body. Even though mitochondria are part of the reason free radicals occur, they’re just as vulnerable to stress and damage from free radicals as anything else. Your mitochondria become weaker and die off as you age. All the not-so-fun aspects of aging – fatigue, fat storage, and decreases in muscle mass and cognitive decline – are all symptoms of impaired mitochondria.

Especially as you age, you want to continue producing new mitochondria to generate as much energy as your cells and organs need and to have enough energy to live the kind of life you want to live.

On the flipside, when you don’t have enough mitochondria, when the ones you have aren’t working well, and when you don’t produce them consistently, you get mitochondrial dysfunction. Mitochondria problems tank your energy levels, and you end up with problems that you wouldn’t expect to have anything to do with your ability to make energy, like cardiovascular disease and obesity.

So, mitochondrial health is a very important aspect of the aging process, and there are different ways that you can help keep your mitochondria healthy. Different ways to promote mitochondrial health are listed in other sections, such as “Growing better mitochondria,” and include exercise, dietary modification/restriction, nutritional supplementation, avoiding environmental toxins, limiting stress, and getting sufficient sleep.

Genetic Eve can help assist you in understanding your Haplogroup and it’s associated risks and providing ideas on protection. Your Family Tree reveals information about your ancestor’s DNA, In particular, your maternal genetics gathered through genetic testing provides valuable information about your mitochondria and it’s sensitivity to toxins.

For the Scientist: A decline in mitochondrial quality and activity has been associated with normal aging and correlated with the development of a wide range of age-related diseases. In particular, mitochondria contribute to specific aspects of the aging process, including cellular senescence, chronic inflammation and an age-dependent decline in stem cell activity. Signaling pathways regulating the mitochondrial unfolded protein response (UPR) and mitophagy also might in turn regulate longevity.

Reactive oxygen species (ROS), unless they are quickly neutralized by antioxidants, can cause considerable damage to mitochondrial membranes and mitochondrial DNA (mtDNA). The injury caused by ROS initiates a self-perpetuating cycle in which oxidative damage impairs mitochondrial function, resulting in the generation of even greater amounts of ROS. Over time, the affected mitochondria become so inefficient, they are unable to generate sufficient energy to meet cellular demands. This is why mitochondria from the cells of older people tend to be less efficient than those from the cells of younger people.

Additionally, mtDNA is not as well protected as nuclear DNA, which is coated with proteins. The “naked” mtDNA becomes an easy target for rogue ROS. In general, as cells age, the numbers of gaps and errors in mtDNA tend to increase, and oxidant exposure is the likely cause. Controlling oxidative damage, therefore, appears to be one strategy for eradicating some of the effects of aging.

“Hot spots” have also been identified in mtDNA in which defects and mutations tend to cluster. Mutations do not appear to be widely distributed in mtDNA; rather, they appear to be clustered in control regions of mtDNA that regulate its replication. Notably, one or more mutations have been observed only in individuals at an advanced age, and some mutations have been found in more than one individual. Most strikingly, a DNA sequence rearrangement has been detected in a generally high proportion of mtDNA molecules in individuals over the age of 65.

The unfolded protein response (UPR) is tightly connected to mitochondria and may also be associated with aging, as mentioned above. This process clears out misfolded proteins so they don’t form aggregates, a term that has been used in relation to neurodegenerative diseases such as Alzheimer’s disease. With aging, this whole process begins to break down.

The first line of defense in the UPR is making more quality control proteins, called chaperones. A badly folded protein will trigger a distress signal, which is sent to the nucleus to recruit more chaperones. However, if the proteins are in such bad shape that the signal isn’t enough, then you need to get rid of these proteins in another way: the proteasome will chew up these degraded proteins to eradicate them.

This process is tightly connected to the mitochondria because it requires cellular energy, so when there’s less energy with age, the process breaks down. Not only the protein production process but also proteins themselves are affected. As you age, proteins accumulate changes as they are exposed to (and modified by) high glucose and high lipids  levels over time. Proteins require maintenance to combat these changes, which is less effective with age.

Current research on mitochondria and aging has tended to focus on several interrelated areas: • Minimizing the generation of compounds that are toxic to mitochondria • Neutralizing and protecting mitochondria from oxidants that are formed • Repairing mitochondrial damage once it has occurred

There are a variety of substances in the body that serve to control mitochondrial damage. These include antioxidants, the enzyme superoxide dismutase (SOD), and uncoupling proteins (UCPs). DNA repair mechanisms also play a role. Scientists are now seeking ways to improve the efficacy of these compounds or processes to reduce the cellular damage associated with mitochondrial damage.

Like many of the health-related issues of aging, decreasing mitochondrial function can ultimately be addressed using a variety of strategies, from lifestyle changes to supplements to drugs. For example, exercise improves mitochondrial function. Likewise, eating a healthy diet is important for mitochondrial health, as eating too much processed or calorie-dense food leads to mitochondrial dysfunction and obesity, which are associated with a variety of other age-related health issues.

Eating healthy and staying active also support autophagy, which is part of the process of clearing out damaged proteins, aggregates, and organelles, including mitochondria. Fasting diets, which have received a lot of attention in the media, have been shown to stimulate autophagy in animal models, but human data is still relatively limited.

Mitochondria and Aging

Image References: