Mitochondria are critical organelles located within your body’s cells that use oxygen to convert food to energy. They play essential roles in metabolism, energy production, intracellular signaling and apoptosis (normal cell death).
Other functions of mitochondria include:
- Detoxification of ammonia in the urea cycle
- Cholesterol metabolism
- Estrogen and testosterone synthesis
- Neurotransmitter metabolism
- Free radical production and detoxification
- Oxidation of fats, carbohydrates and proteins
Mitochondria are found in every cell throughout your body. Cells with high metabolic rates like those in the heart muscle may contain thousands, while cells in low activity areas may contain only a few. Each mitochondrion contains the molecular machinery to manufacture ATP, the energy molecule, via a process called oxidative phosphorylation.
Mitochondria are responsible for generating upward of 90 percent of your body’s ongoing energy needs. When something interferes with normal mitochondrial function, it can have a profound effect on your ability to exercise, think and perform activities of daily living.
What is Mitochondrial Dysfunction?
Environmental signals are continually being sent to your mitochondria to keep you alive. The signals are sent by neurotransmitters and hormones, letting the mitochondria know what to do at any given moment. A certain rare disorder called Mitochondrial DNA Depletion Syndrome (MTDPS), can cause a significant reduction of mitochondrial DNA (mtDNA) and severely limit ATP production.
In the process of burning fuel to produce energy, mitochondria emit free radicals as a part of the oxidative phosphorylation process. Dysfunctional mitochondria produce excessively large amounts of free radicals that emit powerful oxygen atoms. Those atoms can overwhelm the cells, damaging DNA and limiting ATP production.
Antioxidants are chemical compounds that neutralize free radicals and prevent them from damaging cells. The antioxidant defense system in your cells is called the redox system. The redox system generates antioxidants to neutralize free radicals before they can damage cellular components, like DNA and proteins. However, when the mitochondria overproduce free radicals, they may exceed the redox system’s capacity to neutralize them.
Mitochondrial Dysfunction and DNA Damage
DNA is genetic material that carries instructions for the development, function, growth and reproduction of all living organisms. Most DNA is embodied in chromosomes located within a cell’s nucleus. However mitochondria, located in the cytoplasmic fluid that surrounds the cell’s nucleus, have their own DNA, called mtDNA.
Because mitochondria have their own DNA, they are able to replicate themselves and increase in number within a single cell. Physical exercise provides a powerful stimulus for the replication and growth of mitochondria. Restriction of calories through intermittent fasting also stimulates the biogenesis of mitochondria.
Within mtDNA are 37 genes that govern mitochondrial function. Thirteen provide instructions for making ATP, and the remainder are responsible for converting amino acids into usable proteins. When mtDNA is damaged, it causes mitochondrial dysfunction, limiting the cells’ ability to make ATP and perform other metabolic functions.
Mitochondrial Dysfunction and Aging
Mitochondrial dysfunction has been identified as a primary cause of age-related decline. Many aging-related diseases, especially neurodegenerative disorders, involve the mitochondria. Destruction and dysfunction of mitochondria also affect the immune system in older adults, leading to systemic inflammation, vulnerability to common viruses, and reduced function of T-cells, responsible for warding off invading pathogens.
Changes to mitochondria associated with aging include:
- Free radical damage to mitochondrial DNA
- Decreased efficiency in the Krebs cycle that converts glucose to energy
- Reduced ability to meet long term energy demands,
- Enzyme changes that affect cellular respiration
- Free radical production and detoxification
- Decrease in membrane fluidity
Mitochondria play a critical role in healing. Reduced mitochondrial function is closely associated with the slow healing and recovery process observed in older adults. Dysfunctional mitochondria have been shown to play a key role in visual impairment, including age-related macular degeneration.
Drug Toxicity and Mitochondrial Decline
The many metabolic conditions that often plague older adults like diabetes and heart disease may be related to mitochondrial dysfunction. Ironically, the plethora of drugs commonly used to treat those conditions can themselves damage mitochondria. Drug-induced mitochondrial toxicity has been found to cause injury to the liver, muscles, kidneys and central nervous system, and even cause death.
Interventions to reverse mitochondrial damage and restore function are currently at the forefront of research on aging, with many hopeful studies pointing to NAD+ as a potential solution. Nicotinamide adenine dinucleotide, or NAD+, is a co-enzyme found in every cell of your body and vital to mitochondrial health.
NAD+ levels decline as you age, reducing the ability of mitochondria to support energy production. Replenishing NAD+ levels may help slow the aging process and mitigate its debilitating effects on health. NAD+ therapy may be the answer to improving quality of life and prolonging longevity for older adults.
Systems Affected by Mitochondrial Dysfunction
Since mitochondria play a key role in the function of every single cell, dysfunction is capable of derailing any and every physiological process in the human body.
Systems affected by mitochondrial decline include:
- Immune system
The availability of NAD+ declines as we age, partly due to reduced physical activity and nutritional deficits, but also as a natural part of the aging process.
Mitochondrial Dysfunction Symptoms
Dysfunctional mitochondria can produce a broad range of symptoms that affect the cells of multiple systems within your body.
Symptoms of mitochondrial dysfunction may include one or several of the following:
- Chronic fatigue
- Weight loss
- Reduced cognitive function
- Developmental disability (in children)
- Reduced motor control
- Muscle pain and weakness
- Gastrointestinal disorders
- Difficulty swallowing
- Poor endurance
- Poor balance
- Cardiac disease
- Liver disease
- Type II diabetes
- Respiratory problems
- Problems with vision and hearing
- Lactic acidosis
- Susceptibility to infections
- Impaired nervous system
In addition to primary dysfunction, certain degenerative diseases can cause secondary mitochondrial dysfunction, meaning that degradation of the mitochondria is one of the effects of the disease. Those diseases include:
- Alzheimer’s disease
- Muscular dystrophy
- Lou Gehrig’s disease
- Parkinson’s disease
Nicotinamide adenine dinucleotide, or NAD+, is essential to the restoration and repair of mitochondria and mtDNA. Many recent studies present promising findings for reversing mitochondrial decline and stimulating biogenesis.
A 2018 study found that nicotinamide riboside (NR), a precursor to NAD+, increased mitochondrial function in neurons taken from the stem cells of patients with Parkinson’s disease. They also found that NAD+ protects the neurons in Parkinson’s disease fly models. (Schöndorf et al. 2018)
Another 2018 study found that NAD+ improves mitochondrial ATP production and mitochondrial function in rats. (Jing et al. 2018)
In a 2018 report, researchers noted that replenishment of NAD+ levels has beneficial effects for slowing aging and the onset age-related diseases, while expanding lifespan. Mitochondrial restoration was among the reported advantages of NAD+ replenishment. (Aman et al. 2018)
Treatment for Mitochondrial Dysfunction
The unique ability of mitochondria to replicate themselves is often offset by lifestyle behaviors that damage mtDNA. While aging is a natural process, its negative effects can be slowed by making certain behavioral changes.
Physical activity: Because mitochondria are responsible for energy production, they are highly adaptable in response to physical overload. Physical exercise that challenges the muscles, like weight training and vigorous cardiovascular exercise, evokes a mitochondrial response that increases both the size and number of mitochondria in both skeletal and cardiac muscle cells. In addition to promoting mitochondrial health, exercise has numerous benefits that slow aging and enhance quality of life.
Intermittent fasting/caloric restriction: Numerous studies show that restricting your caloric intake and going for long hours between meals stimulates mitochondrial biogenesis. Many specialists recommend intermittent fasting, where your total daily caloric intake is limited to an 8-hour window, followed by 16 hours of fasting. Opt for nutrient-rich plant-based foods, and limit your intake of sugars, grains and processed foods.
NAD+ therapy: NAD+ is a naturally occurring coenzyme derived from Vitamin B3, also called niacin. Because NAD+ is not a drug, it has no harmful side effects and provides multiple health benefits. Oral supplements of nicotinamide riboside (NR) the precursor to NAD+, are available, but they are often poorly absorbed in the digestive system. The most effective way to replenish NAD+ levels is via IV drip.
Mitochondrial Therapy with NAD+ in NYC
Whether you are suffering from the adverse effects of aging or have been diagnosed with a mitochondrial disorder, NAD+ therapy may help restore mitochondrial function and reverse damage to mtDNA.
At Advanced Cryo NYC, we use IV infusion, the most effective method for delivering NAD+. Minimally invasive IV drip therapy bypasses your digestive tract to ensure that potent NAD+ is delivered quickly to your bloodstream and carried to cells throughout your body. Regular NAD+ sessions can boost mitochondrial biogenesis to restore energy pathways and reverse the symptoms of mitochondrial dysfunction.
Don’t resign yourself to the debilitating effects of aging and mitochondrial dysfunction. Contact Advanced Cryo NYC today, and schedule your first NAD+ therapy session https://advancedcryonyc.com/health-and-wellness-contact-us/anti-aging-nad-therapy/ .
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Aman, Yahyah, et al. “Therapeutic potential of boosting NAD+ in aging and age-related diseases.” Translational Medicine of Aging 2 (2018): 30-37.
Canto, Carles, Keir J. Menzies, and Johan Auwerx. “NAD+ metabolism and the control of energy homeostasis: a balancing act between mitochondria and the nucleus.” Cell metabolism 22.1 (2015): 31-53.
Guarente, Leonard. “The resurgence of NAD+.” Science 352.6292 (2016): 1396-1397.
Jing, Ran, et al. “A screen using iPSC-derived hepatocytes reveals NAD+ as a potential treatment for mtDNA depletion syndrome.” Cell reports 25.6 (2018): 1469-1484.
Lee, Chi Fung, et al. “Targeting NAD+ Metabolism as Interventions for Mitochondrial Disease.” Scientific reports 9.1 (2019): 3073.
Schöndorf, David C., et al. “The NAD+ Precursor nicotinamide riboside rescues mitochondrial defects and neuronal loss in ipsc and fly models of parkinson’s disease.” Cell reports 23.10 (2018): 2976-2988.
Verdin, Eric. “NAD+ in aging, metabolism, and neurodegeneration.” Science 350.6265 (2015): 1208-1213.