The mitochondria in your body are known for the ability to generate energy for cells. You may find them referred to as the powerhouse of the body. They also have some other amazing capabilities and play a key role in other life processes.
In fact, the United Mitochondrial Disease Foundation suggests that only 3% of a single mitochondrion’s genetic makeup is designated to produce energy for that single cell.
Mitochondria are organelles in every cell of your body. Each has its own DNA, and they generate up to 90% of cellular energy through the production of adenosine triphosphate (ATP). Mitochondria play a role in every major metabolic function.
Mitochondria are found in varying levels in different tissues, and they are configured to function for their specific tissue. For instance, mitochondria in the liver are configured to transform ammonia into a waste substance called urea. This differentiation of mitochondria demonstrates how environmental and genetic factors can influence their function.
Physiological Effects of the Mitochondria:
- The healthy function of mitochondria is essential to metabolic processes including:
- Synthesizing products necessary for the transportation of glucose and insulin
- Providing sufficient energy for blood flow to and within the heart
- Regulating ion concentrations such as calcium buffering critical to intracellular communication
- Maintain roles in fluctuating lipid levels
- Regulating the removal of cellular damage or apoptosis if the condition is deleterious enough to the mitochondrion’s function.
Dysfunction in mitochondria and your overall health
Research has given us greater insights into the functions of mitochondria that surpass energy production. In fact, the scientific community has a new field of research to specifically investigate how mitochondrial dysfunction negatively affects our health.
Currently, mitochondrial dysfunction is characteristic of a variety of metabolic illnesses and is not categorized as a disease.
A leaky central nervous system
Inflammation of the central nervous system can be activated by an autoimmune response. As a result, specific biomarkers can “leak” away from the central nervous system causing disruption to both the brain and gastrointestinal tract. These inflammatory signals deplete the antioxidant levels linked to the healthy function of mitochondria in the intestines and brain.
The antioxidants spend time neutralizing the compounds that cause inflammation rather than completing their regular functions. For instance, carnitine is an essential amino acid required for producing ATP in the mitochondria. Individuals with autism have been consistently found to have lower levels of carnitine.
Multiple sclerosis
Patients with multiple sclerosis (MS) frequently have impaired ATP synthesis. The lack of ATP is evidence of malfunctioning mitochondria. Most patients with MS exhibit chronic oxidative stress.
Oxidative stress leads to severe health complications by producing excessive free radicals that work to destroy the structure of cells and prevent their proper functioning. Mitochondria are primary targets of oxidative damage because they are the main sites of cellular respiration, which can produce a high amount of free radicals.
Reactive oxygen species (ROS) is a powerful type of free radical that also has a necessary role. ROS is a key player in the function of cells. However, excessive levels deplete beneficial antioxidants such as vitamin C and create destructive changes to the structure of the mitochondrion. The systemic inflammation seen in MS is thought to be a result from excess pro-oxidants known as free radicals.
Autism
Free radical production and damage is one factor at play in illnesses associated with mitochondria dysfunction. Another major implication in the pathogenesis of autism is the transfer of inflammatory signals across the blood-brain barrier.
Abnormal Glutathione Pathways
Glutathione is another antioxidant present in significant levels in the brain. The brains of autistic children have been found to contain abnormal glutathione-producing pathways and reduced glutathione concentrations. Researchers have correlated the levels of glutathione concentrations and oxidative stress to the severity of symptoms associated with autism.
Bipolar disorder
Bipolar disorder is a depressive condition that impacts a person’s mood and behavior. Symptoms of bipolar disorder include an extreme feeling of happiness or sadness, irritability, difficulty sleeping, and the inability to maintain attention.
In addition, people with bipolar disorder are at greater risk of other illnesses such as ulcerative colitis. Although the development of the illness is being investigated in multiple studies, researchers have detected high levels of oxidative stress in these patients. The oxidative stress exacerbates current health complications while creating new problems.
An increase in both reactive oxygen species and similar nitrogen species are often present in cases of chronic oxidative stress. With the increased presence, our body fights back using its own defense system of antioxidants. Patients experiencing other illnesses linked to mitochondria dysfunction including depression and Parkinson’s disease are influenced by significantly low levels of glutathione and thioredoxin systems.
Glutathione is a powerful antioxidant, and the thioredoxin system is a defense system that aids in the removal of both reactive oxygen species and nitrogen species. Combined with glutathione, the two systems are highly efficient at limiting free radical damage and oxidative stress.
Type-2 diabetes
The complexity of mitochondria dysfunction and type-2 diabetes is still being investigated. Questions have been raised whether mitochondria dysfunction may be the cause of type-2 diabetes. Still, scientists believe that type-2 diabetes exacerbates the effects of mitochondria dysfunction.
Metformin, a commonly prescribed drug to treat diabetes, is known to trigger mitochondrial dysfunction and induce conditions that can lead to the development of diabetes. If you are taking metformin, then you are taking a medicine that may actually help keep your body in a diabetic condition.
Chronic fatigue and fibromyalgia
Patients with chronic fatigue syndrome (CFS) and fibromyalgia have detectable changes in the structure of the mitochondria. The mitochondria are composed of different proteins and lipids which contribute to their membranes. The structures of these membranes are important because they help maintain the life cycle of the mitochondria when it grows, splits, or combines with another mitochondrion.
In addition, the membranes of the mitochondria have electron transport chains. The electron transport chain is responsible for oxidative phosphorylation which is the process that creates ATP. Seen in CFS and fibromyalgia, the abnormal mitochondria structure results in a decrease in ATP synthesis.
Cancer
Cancer is also correlated with mitochondria dysfunction. Tumor growth increases due to high rates of cellular respiration. Also, as a result of the high rate of respiration, there is an increased risk of producing free radicals which can react with and harm the mitochondria’s own DNA.
As a result, common mitochondrial DNA mutations that occur increase the development of breast cancer, renal cell carcinoma, and lung cancer.
Heart disease
Heart failure has also been linked to mitochondria dysfunction. The heart requires a constant supply of energy in the form of ATP to perform efficiently. Associated with mitochondria-related myopathy, the heart is a critical organ that is affected by muscle weakness from defective mitochondria.
How to maintain robust mitochondria
Improving the function of your mitochondria can be accomplished by making lifestyle changes. Certain strategies have been shown to treat symptoms associated with defective mitochondria. You can use these techniques beginning today to help you maintain mighty mitochondria.
Intermittent fasting and mitochondria
When the body fasts, malfunctioning mitochondria can become what is called “purged” in a process known as autophagy. Autophagy is a highly important capability for mitochondria to maintain because this ability enables the mitochondria to remove unwanted and damaged debris including accumulated reactive oxygen and nitrogen species as well as unfolded proteins which no longer serve a purpose and can create virus-like problems.
Reduced autophagy of mitochondria has been linked to a higher risk of cancer, Parkinson’s disease, Huntington’s disease, Alzheimer’s disease, and decreased immunity.
Ketogenic diet
A ketogenic diet that is rich in fat and low in carbohydrates has been used to suppress symptoms of muscle weakness and abnormal organ function associated with mitochondria dysfunction. Consuming a ketogenic diet can change the metabolic state by which a body utilizes a specific food source for energy.
Ketones are alternative energy compounds that fuel cells when limited carbohydrates are available. While carbohydrates use the electron transport chain within healthy mitochondria for energy production, fats are broken down by a different process known as the TCA cycle.
The TCA cycle is an efficient energy pathway that the body can use to circumvent defected mitochondria. So effective, a ketogenic diet has been used to treat epilepsy which is a symptom of abnormal mitochondria in the hippocampus region of the brain. A ketogenic diet may also have therapeutic potential in alleviating symptoms associated with mitochondrial myopathy, which presents with a variety of symptoms including muscle weakness.
Exercise daily
Exercise can strengthen the performance of mitochondria in all areas of the body. Exercise reduces oxidative stress when utilized appropriately, and exercise can increase mitochondrial activity by improving oxygen flow and blood pH.
Individuals who run frequently have also been found to have a higher level of functioning mitochondria than those who live sedentary lifestyles.
Nutritional supplementation
The health of our mitochondria depends on our daily diets and the nutrients we consume. For mitochondria to successfully create ATP depends on the structural proteins, enzymes, and other key vitamins in your diet. The following nutrients have been shown to treat mitochondria dysfunction:
Alpha-Lipoic Acid: Alpha-lipoic acid has been especially shown to improve mitochondrial dysfunction in the brain and can improve cognitive ability.
Acetyl-carnitine: Acetyl-carnitine is produced by the body but can also be found in red meat. This amino acid is involved in transporting compounds and also stimulates glutathione production.
B Vitamins: Various B vitamins have been shown to play a critical role in mitochondria function such as biotin and vitamin B-12. B vitamins are highly specialized antioxidants and increase the synthesis of other strong antioxidants such as glutathione.
Coenzyme Q10: Coenzyme Q10 (CoQ) is not only an antioxidant but it is also an essential component of the electron transport chain within the mitochondria. In other words, without CoQ10, there is no synthesis of ATP and therefore a defective mitochondria. Oxidative stress can cause the mitochondrion to over consume any available antioxidants and lead to a deficiency. Depending on the severity of symptoms, CoQ10 supplementation has been shown in studies to help with symptoms associated with CoQ deficiency.
Mitochondrial biogenesis
Mitochondrial biogenesis is the process by which new mitochondria are formed. Researchers are still investigating the series of cell signals that must occur in order for a mitochondrion to either split (fission) or merge (fusion). What is understood is that several environmental influences control the rate and ability at which mitochondria grow and divide including:
- Exercise
- Oxidative Stress
- Temperature
- Caloric restriction
The failure of mitochondrial biogenesis to occur has been implicated as a leading factor for many metabolic problems including diabetes, myopathy, and Alzheimer’s disease. Gaining the ability to control the signals that prompt mitochondria to grow and divide may give doctors the ability to lessen the severity of symptoms related to mitochondrial dysfunction.
Summary
Oxidative stress can impair the function of mitochondria. Exposing your body to environmental contaminants in food, water, air, personal care products and depriving your body of essential nutrients are lifestyle risk factors that you can change.
Feeding oxidative stress promotes further damage to mitochondria which in turn exacerbates illness and cancer. Left untreated, different illnesses and cancers will continue to cause oxidative stress and therefore completes a vicious cycle of deteriorating health.
Promote greater overall health by reducing your risk of mitochondria dysfunction.