{"id":95945,"date":"2020-01-23T08:58:30","date_gmt":"2020-01-23T16:58:30","guid":{"rendered":"https:\/\/selfhacked.com\/?p=95945"},"modified":"2020-07-15T16:25:59","modified_gmt":"2020-07-15T23:25:59","slug":"mitochondrial-dysfunction-disease","status":"publish","type":"post","link":"https:\/\/selfhacked.com\/blog\/mitochondrial-dysfunction-disease\/","title":{"rendered":"Mitochondrial Diseases &#038; Mitochondrial Dysfunction"},"content":{"rendered":"\n<p>Mitochondria turn food into energy for the body. But if they start to malfunction, free radicals can flood the cell, and a number of health problems might arise. Read about the symptoms of mitochondrial dysfunction and the diseases linked to it.  <\/p>\n\n\n<p><!--more--><\/p>\n\n\n<h2><span id=\"Mitochondrial_Dysfunction_Associated_Diseases\"><strong>Mitochondrial Dysfunction &amp; Associated Disease<\/strong>s<\/span><\/h2>\n\n\n\n<h3><span id=\"Recap_Why_Mitochondria_Are_So_Important\">Recap: Why Mitochondria Are So Important <\/span><\/h3>\n\n\n\n<p>Properly functioning mitochondria are central to health, as they are the main energy provider of the cell. However, reactive oxidative species produced by mitochondria accumulate over time, and <strong>oxidative stress leads to age-related diseases<\/strong>. Due to the vast role of mitochondria in the cell, mitochondrial dysfunction is linked to <strong>hundreds of diseases <\/strong>[<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3853754\/\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK27914\/\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3056539\/\">R<\/a>]<strong>.<\/strong><\/p>\n\n\n\n<p>Additionally, a number of metabolic disorders are associated with<strong> genetic mutations<\/strong> in either mitochondrial or nuclear DNA. These mutations may be inherited or occur randomly [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK27914\/\">R<\/a>].<\/p>\n\n\n\n<p>Note that while mitochondrial dysfunction has been observed in or linked to these conditions, it is not necessarily the cause (or even <em>a<\/em> cause). As such, strategies intended to improve mitochondrial function may or may not help manage these diseases. When in doubt, your doctor can help you understand the role of the mitochondria in your health.<\/p>\n\n\n\n<div class=\"sh-summary\"><div class=\"sh-summary-content\">Mitochondria produce energy and remove old, damaged cells. But since the mitochondria use oxygen, their dysfunction can lead to a buildup of cellular waste and free radicals.<\/div><\/div>\n\n\n\n<h3><span id=\"1_Cancer_Research\"><strong>1) Cancer Research<\/strong><\/span><\/h3>\n\n\n\n<p>Cancer cells require mitochondria to power the growth of tumors. Cancer cells tend to have an increased number of mitochondria to provide this energy. The mitochondrial increase is mediated independently by different transcription factors or proteins that initiate the production of specific genes [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3853754\/\">R<\/a>].<\/p>\n\n\n\n<p>On the other hand, cancer cells increase the turnover of mitochondria that have accumulated free radicals. <strong>Oxidative stress is increased in cancer cells, which<\/strong> damages the surrounding tissue [<a href=\"http:\/\/www.cell.com\/fulltext\/S0092-8674(16)30908-4\">R<\/a>].<\/p>\n\n\n\n<p>One of the hallmarks of cancer is the ability of the cell to<strong> avoid programmed cell death <\/strong>(<strong>apoptosis<\/strong>). Normally, the mitochondria of healthy cells would trigger this process if the cell was replicating too much or too quickly. However, in cancer cells, programmed cell death is avoided by increasing the destruction of mitochondria that have accumulated free radicals. They also turn on antioxidant pathways so that oxidative stress does not trigger cell death [<a href=\"http:\/\/www.cell.com\/fulltext\/S0092-8674(16)30908-4\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3853754\/\">R<\/a>].<\/p>\n\n\n\n<p>Mitochondria of cancer cells have lower levels of proteins that promote cell death (<a href=\"https:\/\/selfdecode.com\/gene\/bax\/?utm_source=seo&#38;utm_medium=selfhacked&#38;utm_campaign=id00002\">BAX<\/a>\/BAK) and\/or higher levels of proteins that prevent cell death (<a href=\"http:\/\/selfdecode.com\/gene\/bcl2\/?utm_source=seo&#38;utm_medium=selfhacked&#38;utm_campaign=id00002\">BCL-2<\/a>\/BCL-XL) [<a href=\"http:\/\/www.cell.com\/fulltext\/S0092-8674(16)30908-4\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3853754\/\">R<\/a>].<\/p>\n\n\n\n<p>The network of mitochondria in cancer cells is also different. Cancer cells have more <strong>fragmented mitochondria<\/strong> (by increasing mitochondrial division and decreasing fusion) [<a href=\"http:\/\/www.cell.com\/fulltext\/S0092-8674(16)30908-4\">R<\/a>].<\/p>\n\n\n\n<p>Cancer cells also produce energy differently through a process known as the <strong>Warburg effect<\/strong>. Energy production is largely done without oxygen (anaerobically), via glycolysis. This may be caused by turning down mitochondrial function to avoid apoptosis [<a href=\"http:\/\/www.cell.com\/fulltext\/S0092-8674(16)30908-4\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3853754\/\">R<\/a>].<\/p>\n\n\n\n<p>Aerobic respiration through the Krebs cycle and oxidative phosphorylation still occur in cancer cells but to a lesser degree.<\/p>\n\n\n\n<div class=\"sh-summary\"><div class=\"sh-summary-content\">Scientists think that mitochondrial dysfunction may play a role in cancer, but this hasn\u2019t been sufficiently proven.<\/div><\/div>\n\n\n\n<h3><span id=\"2_Neurodegenerative_Diseases\"><strong>2) Neurodegenerative Diseases<\/strong><\/span><\/h3>\n\n\n\n<p>Mitochondrial dysfunction is a large cause of age-related neurodegenerative diseases like Alzheimer\u2019s, ALS, and Parkinson\u2019s disease. The accumulation of free radicals with age results in<strong> DNA and protein damage<\/strong>. Mitochondria <strong>accumulate defective proteins<\/strong> that cause loss of energy production and ultimately cell death [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3056539\/\">R<\/a>].<\/p>\n\n\n\n<p>The mitochondria have been observed to behave differently (to be dysfunctional) in specific neurodegenerative diseases like Alzheimer\u2019s and Parkinson\u2019s.<\/p>\n\n\n\n<h4><strong>Alzheimer\u2019s Disease<\/strong><\/h4>\n\n\n\n<ul><li>Amyloid beta proteins build up around the outer mitochondrial membrane.<\/li><li>This buildup decreases ATP production, increases oxidative stress, and ultimately causes cell death.<\/li><li>Amyloid beta increases mitochondrial protein production.<\/li><li>Mitochondrial enzymes have decreased activity, leading to reduced ATP levels.<\/li><li>Mitochondria undergo structural changes within the cell. Rather than existing in long tubes (mitochondrial fusion), the mitochondria are fragmented into little pieces within the cell (fission). This adds to the overall dysfunction of brain cells seen in patients with Alzheimer\u2019s disease [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3056539\/\">R<\/a>].<\/li><\/ul>\n\n\n\n<h4><strong>Parkinson\u2019s Disease<\/strong><\/h4>\n\n\n\n<ul><li>The hallmark of Parkinson\u2019s is the accumulation of alpha-synuclein protein, leading to cell death and loss of neurons.<\/li><li>Patients with Parkinson\u2019s accumulate this protein in the mitochondria, leading to increased oxidative stress and reduced energy production.<\/li><li>Parkin protein (E3 ubiquitin ligase) and PINK1 protein are responsible for marking damaged mitochondria for destruction. Patients with Parkinson&#8217;s disease have low levels of these proteins.<\/li><li>Damaged, low functioning mitochondria are not degraded and remain in the cell.<\/li><li>Alpha-synuclein continues to accumulate, leading to neurodegeneration [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5361502\/\">R<\/a>].<\/li><\/ul>\n\n\n\n<div class=\"sh-summary\"><div class=\"sh-summary-content\">Mitochondrial dysfunction is implicated in the brain changes characteristic of Alzheimer\u2019s and Parkinson\u2019s disease.<\/div><\/div>\n\n\n\n<h3><span id=\"3_Diabetes\"><strong>3) Diabetes<\/strong><\/span><\/h3>\n\n\n\n<p>Improper mitochondrial function has been seen in patients with both type 1 and type 2 diabetes. Aside from having a lack of glucose for respiration, the<strong> network and shape<\/strong> of mitochondria in the cells of diabetic patients may be abnormal [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2824521\/\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3853754\/\">R<\/a>].<\/p>\n\n\n\n<p>In diabetic patients, the mitochondria are broken up into small fragmented networks (increased division, decreased fusion) throughout the cell. This has been observed in both type 1 and type 2 diabetes [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2824521\/\">R<\/a>].<\/p>\n\n\n\n<p>Type 2 diabetes is characterized by insulin resistance in cells, reducing the amount of glucose available for respiration. This decreases ATP production and thus the energy available to the cell [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2824521\/\">R<\/a>].<\/p>\n\n\n\n<p>It is unknown whether mitochondrial dysfunction is a cause of insulin resistance or a symptom of it. Some researchers have suggested that <strong>mitochondrial dysfunction could be a cause of insulin resistance<\/strong>, rather than a symptom [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2824521\/\">R<\/a>].<\/p>\n\n\n\n<p>Patients with type 2 diabetes have reduced levels of mitochondrial proteins responsible for energy production [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2824521\/\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3853754\/\">R<\/a>].<\/p>\n\n\n\n<div class=\"sh-summary\"><div class=\"sh-summary-content\">Type 2 diabetes might be marked by poor mitochondrial function, but more research is needed to confirm this.<\/div><\/div>\n\n\n\n<aside class=\"sh-partner shp-form sponsored sh-et-7388fa\">\n  <div>\n          <div class=\"partner-heading\">8 Ways To Use Your DNA &amp; Optimize Your Health<\/div>\n    \n    <div class=\"partner-content\">\n      <p><span style=\"font-weight: 400\">What kinds of secrets could your genes hold? Read this guide and find out how you can take your health into your own hands and find the root cause of your issues through gene-based health.<\/span><\/p>\n    <\/div>\n\n    <div class=\"subscribe-form-container\">\n      <form method=\"POST\" action=\"\/wp-json\/wp\/v2\/posts\/95945\" class=\"sh-subscribe-form\">\n        <input type=\"email\" name=\"subscribe_form_data[email]\"\n            pattern=\"^[a-zA-Z0-9.!#$%&\u2019*+\/=?^_`{|}~-]+@[a-zA-Z0-9-]+(?:\\.[a-zA-Z0-9-]+)*$\" required\n            placeholder=\"Enter your email\">\n                  <input type=\"hidden\" name=\"subscribe_form_data[tags][]\" value=\"SH Optin: PartnerAd Your DNA Your Health\">\n                  <input type=\"hidden\" name=\"subscribe_form_data[tags][]\" value=\"SH Optin: Your DNA Your Health Guide\">\n                  <input type=\"hidden\" name=\"subscribe_form_data[tags][]\" value=\"PartnerAd\">\n                <button type=\"submit\" class=\"btn btn-primary subscribe-submit\">Optimize My Health<\/button>\n      <\/form>\n    <\/div>\n  <\/div>\n          <style>aside.sponsored.sh-et-7388fa::before{content:\"Advertisement\"}<\/style>\n<\/aside>\n<h3><span id=\"4_Heart_Failure\"><strong>4) Heart Failure<\/strong><\/span><\/h3>\n\n\n\n<p>Heart cells rely heavily on mitochondria to power the pumping of the heart. Mitochondrial dysfunction is implicated in<strong> heart failure<\/strong> due to the buildup of oxidative stress [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3853754\/\">R<\/a>].<\/p>\n\n\n\n<p>Patients with heart failure exhibit reduced mitochondrial activity. The mitochondria have lower activity at electron transport chains. This is caused by a <strong>loss of oxygen supply<\/strong> to the mitochondria [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3853754\/\">R<\/a>].<\/p>\n\n\n\n<p>Since oxygen supply is reduced, electrons at the electron transport chain cannot be picked up by oxygen. This leads to the<strong> accumulation of electrons,<\/strong> which produce free radicals [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3853754\/\">R<\/a>].<\/p>\n\n\n\n<h3><span id=\"5_Chronic_Fatigue_Syndrome\"><strong>5) Chronic Fatigue Syndrome<\/strong><\/span><\/h3>\n\n\n\n<p><a href=\"https:\/\/selfhacked.com\/blog\/my-cutting-edge-protocol-to-cure-fatigue\/\">Chronic Fatigue<\/a> Syndrome, commonly known as CFS, is a controversial and lifelong disorder characterized by prolonged (over 6 months) symptoms of intense fatigue that can <strong>reduce a person\u2019s ability to perform daily functions by over 50%<\/strong>. Patients with CFS suffer from a variety of other symptoms including [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2766938\/\">R<\/a>]:<\/p>\n\n\n\n<ul><li><a href=\"https:\/\/selfhacked.com\/blog\/natural-treatments-anxiety\/\">Anxiety<\/a><\/li><li><a href=\"https:\/\/selfhacked.com\/blog\/natural-treatments-depression\/\">Depression<\/a><\/li><li><a href=\"https:\/\/selfhacked.com\/blog\/natural-treatment-migraines\/\">Headaches<\/a><\/li><li>Muscle <a href=\"https:\/\/selfhacked.com\/blog\/23-ways-to-combat-pain-naturally-by-increasing-your-opioids\/\">Pain<\/a><\/li><li><a href=\"http:\/\/selfhacked.com\/blog\/the-cause-of-brain-fog\/\">Cognitive Dysfunction<\/a><\/li><\/ul>\n\n\n\n<p>Although it was once thought to be a disease of the mind, increasing evidence points to mitochondrial dysfunction as one of the <strong>leading possible causes<\/strong> of this disorder [<a href=\"http:\/\/www.ijcem.com\/files\/IJCEM1204005.pdf\">R<\/a>].<\/p>\n\n\n\n<p>Multiple clinical trials have been conducted and have <strong>produced mixed results<\/strong>. According to some researchers, CFS may be linked to one or more of the following mitochondrial abnormalities [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC4136529\/table\/t0010\/\">R<\/a>]:<\/p>\n\n\n\n<ul><li>Smaller mitochondrial shape and number<\/li><li>Lower L-carnitine, <a href=\"http:\/\/selfhacked.com\/blog\/top-18-science-based-health-effects-carnitine\/\">ALCAR<\/a>, ubiquinone or <a href=\"https:\/\/selfhacked.com\/blog\/coenzyme-q10-ubiquinol\/\">CoQ10<\/a> levels<\/li><li>Reduced protein activity in the electron transport chain (oxidative phosphorylation)<\/li><li>Reduced ATP production<\/li><\/ul>\n\n\n\n<p>A number of studies indicated that there were<strong> no significant differences<\/strong> in mitochondrial structure or function of healthy and normal patients. Further studies are required to fully understand the cause of this condition, the role of mitochondrial dysfunction and how to effectively treat patients.<\/p>\n\n\n\n<div class=\"sh-summary\"><div class=\"sh-summary-content\">A link between mitochondrial dysfunction and chronic fatigue syndrome has been proposed but never confirmed.<\/div><\/div>\n\n\n\n<h3><span id=\"6_Genetic_Disorders\"><strong>6) Genetic Disorders<\/strong><\/span><\/h3>\n\n\n\n<p>Genetic mutations in mitochondrial genes can result in mitochondrial dysfunction through <strong>1 or more of 5 <\/strong>distinct mechanisms [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK27914\/\">R<\/a>]:<\/p>\n\n\n\n<ul><li>Inability to utilize other molecules (substrates) for energy production<\/li><li>Improper Krebs cycle<\/li><li>Defective energy production through the electron transport chain (oxidative phosphorylation)<\/li><li>Defective transport of molecules in and out of the mitochondria<\/li><li>Defective proteins in the electron transport chain<\/li><\/ul>\n\n\n\n<p>These defects can be caused by mutations in mitochondrial and\/or nuclear DNA. Additionally, defects can occur when mitochondrial DNA is unable to communicate with nuclear DNA [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK27914\/\">R<\/a>].<\/p>\n\n\n\n<p>Some metabolic diseases that are caused by mitochondrial and\/or nuclear DNA mutations include [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK27914\/\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3853754\/\">R<\/a>]:<\/p>\n\n\n\n<ul><li><strong>mtDNA depletion syndrome <\/strong>(<strong>MDS<\/strong>): MDS refers to a group of disorders, any of which have dysfunctional mitochondrial DNA. This can result in different developmental, muscle, and brain abnormalities. Many known mitochondrial diseases are a result of MDS.<\/li><li><strong>Mitochondrial myopathy<\/strong>: a Mitochondrial disease that causes muscle problems such as weakness, <a href=\"https:\/\/selfhacked.com\/blog\/top-14-proven-health-benefits-exercise-references-mechanisms\/\">exercise<\/a> intolerance, breathing difficulties, or issues with vision.<\/li><li><strong>Mitochondrial encephalomyopathy<\/strong>,<strong> lactic acidosis<\/strong>,<strong> and <\/strong>stroke<strong>-like episodes <\/strong>(<strong>MELAS<\/strong>): A mitochondrial disorder that affects the brain and muscle throughout the body. Stroke-like episodes and the buildup of <a href=\"http:\/\/selfhacked.com\/blog\/the-brains-secret-backup-generator\/\">lactic acid<\/a> results in dementia, vomiting, extreme <a href=\"https:\/\/selfhacked.com\/blog\/23-ways-to-combat-pain-naturally-by-increasing-your-opioids\/\">pain<\/a>, and muscle weakness.<\/li><li><a href=\"https:\/\/selfhacked.com\/blog\/coenzyme-q10-ubiquinol\/\"><strong>CoQ10<\/strong><\/a><strong> deficiency<\/strong>: A deficiency in <a href=\"https:\/\/selfhacked.com\/blog\/coenzyme-q10-ubiquinol\/\">coenzyme Q10<\/a>, a protein that is part of the electron transport chain.<\/li><li><strong>Mitochondrial neurogastrointestinal encephalomyopathy <\/strong>(<strong>MNGIE<\/strong>): A rare mitochondrial disease that primarily affects the brain and digestive system. The muscles and nerves of the digestive system do not properly push food through the system.<\/li><li><strong>Mitochondrial diabetes<\/strong>: Referred to as maternally inherited diabetes and deafness (MIDD), a subtype of diabetes caused by a single mutation in the mitochondrial DNA (at position 3243). The disease results in loss of hearing and diabetes similar to type 1.<\/li><li><strong>POLG mutations<\/strong>: A gene that codes for DNA polymerase subunit gamma, the active (catalytic) part of the mitochondrial protein responsible for DNA synthesis. Mutations in this gene lead to the defective production of mitochondrial proteins and many mitochondrial diseases.<\/li><\/ul>\n\n\n\n<div class=\"sh-summary\"><div class=\"sh-summary-content\">Various mutations in mitochondrial genes can result in mitochondrial dysfunction and an array of metabolic diseases.<\/div><\/div>\n\n\n\n<h4><strong>The Mitochondrial Bottleneck Effect<\/strong><\/h4>\n\n\n\n<p>Carrying mutations in mitochondrial DNA <strong>does not necessarily mean that you will transmit the disease.<\/strong> According to some researchers, the proportion of cells carrying mutated mitochondria may have to be significantly higher than the cells carrying healthy mitochondria in order for the disease to present symptoms [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2777314\/\">R<\/a>].<\/p>\n\n\n\n<p>During female egg cell (oocyte) production, each egg cell will carry a random selection of mitochondrial DNA copies. Some of the copies may carry mutations, whereas some may be completely normal. As the egg cell matures and prepares for fertilization, many mitochondria are replicated at random. This may dilute the chance of inheriting mutant mitochondria [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2777314\/\">R<\/a>].<\/p>\n\n\n\n<p>This phenomenon means that if the mother carries highly mutant mitochondria, her offspring will not necessarily carry the trait [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2777314\/\">R<\/a>].<\/p>\n\n\n\n<p>If enough cells carry mutant mitochondrial DNA &#8211; for example, more than 50% of the cells in the body &#8211; it is likely that the child will have the associated disorder.<\/p>\n\n\n\n<h4><strong>Preventing Inheritance of Dysfunctional Mitochondrial DNA (mtDNA)<\/strong><\/h4>\n\n\n\n<p>New technologies can prevent the transmission of mutated mitochondrial DNA from the mother to the offspring. A new technique, called<strong> 3-parent <em>in vitro fertilization<\/em><\/strong>, consists of switching nuclear DNA from the mother with the nuclear DNA of a donor female egg that has healthy mitochondrial DNA. Therefore, the donor egg carries the genetic information from the mother but lacks the mutated mitochondrial DNA that she carries as well.<\/p>\n\n\n\n<p>Using in vitro fertilization, the egg is then artificially inseminated using the paternal <a href=\"https:\/\/selfhacked.com\/blog\/unhealthy-ejaculate\/\">semen<\/a>. The fertilized egg is then reintroduced into the mother&#8217;s uterus, where it can latch on to the uterus [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC4005382\/\">R<\/a>].<\/p>\n\n\n\n<p>The offspring will have all of the physical characteristics of their biological parents because the nuclear DNA is unchanged. The only thing that is different is that this child will have proper mitochondrial function, unlike the mother who carries mutated copies of the mitochondrial DNA [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC4005382\/\">R<\/a>].<\/p>\n\n\n\n<h2><span id=\"Possible_Signs_Symptoms_of_Mitochondrial_Dysfunction\"><strong>Possible Signs &amp; Symptoms of Mitochondrial Dysfunction<\/strong><\/span><\/h2>\n\n\n\n<p>Some researchers have identified possible signs that the mitochondria are not functioning as they should. These include:<\/p>\n\n\n\n<ul><li>Feeling excessively tired [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC4136529\/\">R<\/a>]<\/li><li>Inability to exercise for long periods of time [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3526786\/\">R<\/a>]<\/li><li>Shortness of breath, especially during exercise [<a href=\"http:\/\/erj.ersjournals.com\/content\/12\/3\/742\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3197343\/\">R<\/a>]<\/li><li>Poor bone growth and health [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/28899781\">R<\/a>]<\/li><li>Difficulty controlling movements, balance, and coordination (ataxia) [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/21827900\">R<\/a>]<\/li><li>Difficulty walking or talking [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3565683\/\">R<\/a>]<\/li><li>Muscle weakness and pain [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3581062\/\">R<\/a>]<\/li><li>Heart muscle disease (cardiomyopathy) [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3783139\/\">R<\/a>]<\/li><li>Gut and digestive issues [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5330602\/\">R<\/a>]<\/li><li>Liver and kidney disease [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3888320\/\">R<\/a>]<\/li><li>Droopy eyelids, vision loss, and other eye problems [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3652603\/\">R<\/a>]<\/li><li>Diabetes and other hormonal disorders [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2824521\/\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/23769710\">R<\/a>]<\/li><li>Trouble hearing [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/16120424\">R<\/a>]<\/li><li><a href=\"http:\/\/selfhacked.com\/blog\/natural-treatment-migraines\/\">Migraines<\/a>, strokes, and seizures [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/24331360\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/19268975\">R<\/a>]<\/li><li>Difficulty remembering things [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/19268975\">R<\/a>]<\/li><li>Developmental delay [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/10641610\">R<\/a>]<\/li><li>Autism [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/12174964\">R<\/a>]<\/li><li>Recurrent infections [<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/20509844\">R<\/a>, <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3097475\/\">R<\/a>]<\/li><\/ul>\n\n\n\n<p>Note that these symptoms may have many causes other than mitochondrial dysfunction. In fact, <strong>they are more likely to be associated with another diagnosable and treatable health problem<\/strong>, which your doctor can identify and address.<\/p>\n\n\n\n<p>If you are currently suffering from symptoms such as these, and they are not currently being addressed, <strong>we strongly recommend talking to a doctor to determine the best treatment or management plan for your health.<\/strong><\/p>\n\n\n\n<div class=\"sh-summary\"><div class=\"sh-summary-content\"><\/p>\n\n\n\n<h3><span id=\"Takeaway\">Takeaway<\/span><\/h3>\n\n\n\n<p>Mitochondria produce energy (ATP), recycle parts of cells that can be reused, and remove cells that are old and damaged beyond repair. <\/p>\n\n\n\n<p>But since the mitochondria use oxygen, an excess of their byproducts can cause oxidative stress. When mitochondria break down, free radicals and cellular waste can flood cells and cause harm. <\/p>\n\n\n\n<p>Mutations in mitochondrial genes can result in mitochondrial dysfunction and an array of metabolic diseases. Mitochondrial dysfunction is also implicated in neurodegenerative diseases like Alzheimer\u2019s diseases and chronic diseases like diabetes and heart failure.  <\/p>\n\n\n\n<p>The symptoms of mitochondrial dysfunction can greatly vary from person to person and may include fatigue, shortness of breath, coordination issues, and neurological problems, among others.<\/div><\/div>\n\n\n\n<h3><span id=\"Further_Reading\">Further Reading<\/span><\/h3>\n\n\n\n<ul><li><a href=\"https:\/\/selfhacked.com\/blog\/mitochondria\/\">What Are Mitochondria? Definition, Function &amp; Structure<\/a><\/li><\/ul>\n","protected":false},"excerpt":{"rendered":"<p>Mitochondria turn food into energy for the body. But if they start to malfunction, free radicals can flood the cell, and a number of health problems might arise. Read about the symptoms of mitochondrial dysfunction and the diseases linked to it.  <\/p><\/p>\n","protected":false},"author":26632,"featured_media":95950,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":[],"categories":[90,359],"tags":[434,33893],"yst_prominent_words":[33882,907,763,1199,33883,13261,1554,6943,6646,13260,6643,33900,33898,13263,816,511,33899,33897,33881,1076],"_links":{"self":[{"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/posts\/95945"}],"collection":[{"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/users\/26632"}],"replies":[{"embeddable":true,"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/comments?post=95945"}],"version-history":[{"count":16,"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/posts\/95945\/revisions"}],"predecessor-version":[{"id":110454,"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/posts\/95945\/revisions\/110454"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/media\/95950"}],"wp:attachment":[{"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/media?parent=95945"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/categories?post=95945"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/tags?post=95945"},{"taxonomy":"yst_prominent_words","embeddable":true,"href":"https:\/\/selfhacked.com\/wp-json\/wp\/v2\/yst_prominent_words?post=95945"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}