The mitochondria is the â€œpowerhouse of the cellâ€. It obtained this nickname by being the creator of ATP, or the energy our body produces to carry out functions. However, the mitochondria is responsible for so much more than that. More recently, studies have been showing a link between mitochondrial health and degenerative age-related diseases such as type 2 diabetes, Alzheimerâ€™s, and others. Mitochondrial dysfunction can be linked and grouped into three categories: neurodegenerative diseases, immune diseases, and hepatic diseases.Â
More About Mitochondria
Way back when, it is believed that a large prokaryotic organism ingested mitochondria and rather than digesting them, decided to keep them around due to the increased amount of energy they received and their new ability to take in oxygen. The mitochondria is also the only organelle that possesses its own DNA. Mitochondrial DNA is highly important as it codes specific enzymes that allow the mitochondria to properly function.Â
The mitochondria make fuel for the body. Part of making this fuel requires oxygen. This is where the foods we take in like sugars and fats are burned in the presence of oxygen on the way to forming ATP. The leftover hydrogen ions are built up in the intermembrane and slow down the flow of the electron transport chain (ETC). During this process,Â the mitochondria also produce â€œwasteâ€. The waste is referred to as hydroxyl radical, the superoxide radical and hydrogen peroxide. All of these elements are toxic to the mitochondria if they build up too high.Â
Mitochondria and Oxidative Stress
If we consider degenerative diseases, we can see that the level of antioxidants one processes and their enzymes are reduced. This damage is progressive and is thought to occur because of damage and dysfunction regarding the cellâ€™s mitochondria. Eventually, the cell can not make enough energy, which leads to other issues throughout the body, inflammation, and a diagnosis.Â
Those who suffer from chronic health conditions typically have lived an unhealthy lifestyle involving working too hard, or they have been under copious amounts of stress for long periods of time, they are mainly sedentary, do not eat well, or have had exposure to toxins. When our body is under these conditions it puts a significant strain on the mitochondria. This creates a build-up of free radicals.Â
Overtime, the mitochondria begin to dysfunction. As the levels of free radicals increase, the damage to the mitochondrial membrane gets worse. Next, the enzymes are damaged and mutations occur in the mitochondrial DNA, leaving the mitochondria to produce little energy. The mitochondria themselves develop toxicity and when the mitochondria sense these things, it undergoes apoptosis.Â
If this happens over and over again patients suffer from organ dysfunction. An example of this is peripheral neuropathy. When the peripheral nerve cells are exposed to an increasing amount of oxidative stress, the result is young nerve fibers die. This leaves patients with pain in their extremities.Â
Â The brain and nervous system have a lot to do with mitochondria as they use up about 25-30% of the bodyâ€™s energy created. Additionally, if these are impacted and you have inflammation or an infection, the immune system uses leftover energy as well.Â
For more information regarding the link between mitochondrial dysfunction and neurodegenerative diseases, please review this article:Â
â€œGuidelines on Experimental Methods to Assess Mitochondrial Dysfunction in Cellular Models of Neurodegenerative Diseaseâ€Â
Testing Mitochondrial HealthÂ
There are a few ways that we are able to test mitochondrial health. The first being an oxidative stress profile from Genova. This test includes specific markers that can also be used to determine the effectiveness of our mitochondria. A sample test is shown below:Â
Second, there is a Micronutrient test by SpecraCell. This test allows us to see the energy production, micronutrients you may be lacking in, and how it is effecting your Krebs cycle and ultimately your ATP production. A sample is shown below:Â
In order to best help our mitochondria and support them, we need to first look at the diet and our genes. Our diet is responsible for many of the micronutrients needed to properly execute cellular functions. Everything begins in the kitchen, ultimately leading to mitochondrial health as well as genetic support.Â
Acetyl-L-Carnitine is though to be a natural stimulant for the mitochondria. We can naturally improve these numbers in our body by eating foods such as local, organic grass-fed beef, chicken, and milk.Â
It is key to feed our cells these nutrients to resist mitochondrial dysfunction. If we do not properly feed our genes, they will alter, leading to compromised immune function and expression.Â
For more information regarding the expression of the SESN2 gene and mitochondrial dysfunction, please visit:Â
â€œMitochondrial Dysfunction Induces SESN2 Gene Expression Through Activating Transcription Factor 4â€
We are realizing more than everything starts with the kitchen. The ingredients we put into our mouth will ultimately affect our energy production, our genetics, our immune system, and so much more! It is critical to understand that the food you feed yourself and your children, could be the determining factor in their health down the road. We have the ability and chance to make positive steps in the right direction now and reduce inflammation and mitochondrial dysfunction. Take the steps now to reduce your risk of neurodegenerative diseases and other chronic health conditions. -Kenna Vaughn, Senior Health CoachÂ
Garaeva AA, Kovaleva IE, Chumakov PM, Evstafieva AG. Mitochondrial dysfunction induces SESN2 gene expression through Activating Transcription Factor 4. Cell Cycle. 2016;15(1):64â€71. doi:10.1080/15384101.2015.1120929Â
Kaiser, Jon. â€œA Clinician’s Guide to Mitochondrial Medicine.â€ Functional Medicine University. 2020, www .functionalmedicineuniversity .com/members/1041.cfm.
Connolly NMC, Theurey P, Adam-Vizi V, et al. Guidelines on experimental methods to assess mitochondrial dysfunction in cellular models of neurodegenerative diseases. Cell Death Differ. 2018;25(3):542â€572. doi:10.1038/s41418-017-0020-4Â
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