Why do We Care About the Health of Our Mitochondria?
As we learned in Part I, mitochondria are more than just the powerhouses of the cell – they are the production line workers, making hormones and energy; the CEOs, telling other cells what to do and when; the HR department, letting certain cells go, and encouraging others to quit; and the floor managers, telling certain molecules where to be within the cell. When they’re working well, life is good. When they’re working optimally, life is really good! But when they start to slack, making less energy, making energy but less efficiently, or communicating poorly, we suffer in many ways.
What happens when they don’t work?
Altered mitochondrial functioning is characteristic of aging and virtually all chronic disease.(1) Mitochondrial dysfunction has been linked to a wide variety of conditions, including, but not limited to:
- Chronic fatigue syndrome/myalgic encephalomyelitis (2)
- Fibromyalgia (3)
- Autoimmune conditions, such as systemic lupus erythematosus (4), type I diabetes (5), multiple sclerosis (6, 7)
- Type II diabetes (5)
- Cardiovascular conditions, such as cardiomyopathy, endothelial dysfunction, conduction defects, and coronary artery disease (8)
- Neurodegenerative disorders, such as Alzheimer’s (9,10), Parkinson’s (10, 11), amyotrophic lateral sclerosis (12)
- Cancer (13, 14)
- Autism spectrum disorders (15)
- Psychiatric conditions such as bipolar disorder (16, 17), depression (18, 19), schizophrenia (17, 20)
In certain health conditions, such as Alzheimer’s, research has shown mitochondrial oxidative damage to be the earliest cellular abnormality in the development of the disease, indicating that mitochondrial dysfunction may be at the root of certain diseases.(21) In other conditions, such as Autism spectrum disorders (ASD), there is some debate as to whether the mitochondrial dysfunction occurs primarily, or is the result of dysfunction elsewhere, such as within the immune system or calcium signaling pathways.(22) Regardless, mitochondrial dysfunction appears to occur at some point in the biochemical cascade within the progression of most, if not all, diseases.
It is theorized that mitochondrial damage is at the root of why we age, and progressive mitochondrial decay may be why we can’t live forever.(23) Impairment of enzymes, enhanced reactive oxygen species (ROS) production, mutations within the mitochondrial DNA, reduction of antioxidants, increased accumulation of damaged mitochondria (due to impaired phagocytosis), and defective electron transport chains are all thought to be contributors of mitochondrial-driven aging and disease. (23,24,25) These alterations in function cause the mitochondria to behave inefficiently, producing less NAD in comparison to how much NADH is hanging around in the mitochondria. If we are aging prematurely, are chronically sick, or have chronic pain, we are experiencing a decreased NAD/NADH ratio, and decreased ATP (energy) production; the mitochondria are acting inefficiently.
Due to the vital role of ATP production, even a mild decrease in mitochondrial dysfunction may lead to symptoms; if you are experiencing low energy, food cravings, difficulty focusing, forgetfulness, an afternoon energy slump, muscle weakness, exhaustion after mental or physical exertion, hormonal imbalances, or pain, your mitochondria may not be working efficiently.
What determines whether or not we have efficient mitochondria?
Many, many different factors. But there’s good news – many of them are factors that we can control! The fate of your mitochondria is not predetermined. Join us for Part 3 to learn about the causes of mitochondrial dysfunction.