Summary
In this episode of The Peter Atia Drive, Peter Atia explains why the podcast does not run ads and instead relies on listener support. The guest on this episode is Dr. MC Muta, a professor of systems biology at Harvard Medical School who specializes in rare mitochondrial diseases. The conversation delves into the history of mitochondria and how they came to exist through endosymbiosis, a process where one organism lives inside another and eventually becomes a part of it. The conversation then explores the genetic makeup of mitochondria and their role in causing diseases. The podcast discusses the signals that lead to an increase in mitochondrial biogenesis in muscle cells during exercise. The context discusses the role of mitochondria in energy transformations and the generation of ATP. The speaker discusses the hypothesis that mitochondrial damage leads to an increase in inflammation in the body as the immune system confuses mitochondrial DNA with bacterial DNA. The speaker discusses their testing methods, including lactate testing, and their interest in studying the effects of metformin on individuals with diabetes. The conversation revolves around Li syndrome, a disease caused by the loss of a subunit of complex one in the mitochondria. The conversation discusses the potential link between mitochondrial dysfunction and Parkinson's disease.
The speaker initially wanted to become a doctor but fell in love with math in high school and went on to study math and computer science at Stanford. The speaker then became interested in mitochondrial disorders and now runs a research group focused on developing new diagnostics and drugs for these patients. The podcast also provides a basic overview of mitochondria and the process of cellular energy production from glucose. The context discusses mitochondrial mutations and their impact on neurodegenerative diseases. The speaker discusses the potential therapeutic benefits of hypoxia, particularly in individuals with mitochondrial disorders. The conversation also explores the potential for targeting mitochondrial proteins as therapies for mitochondrial disease, including the use of protein prostheses. The conversation ends with a discussion about the potential for enhancing mitochondrial performance for athletic performance, but the complexity of the system makes it unlikely to be achieved through a single molecule.
The conversation discusses the potential link between mitochondrial dysfunction and Parkinson's disease. The speaker shares a study that found that exercise with antioxidants may prevent some of the beneficial effects of exercise, as reactive oxygen species play an important signaling role in the adaptation process. The discussion then shifts to the topic of metformin and its potential impact on exercise and mitochondrial function. The podcast ends with a discussion on the cost of lactate meters and strips. The context is about diagnosing patients with mitochondrial disease through measuring their oxygen extraction while on a treadmill. The speaker notes that while there is compelling evidence that exercise is beneficial, it is difficult to determine the optimal type and amount of exercise for longevity.
The conversation discusses the potential for targeting mitochondrial proteins as therapies for mitochondrial disease, including the use of protein prostheses. The conversation also explores the potential for enhancing mitochondrial performance for athletic performance, but the complexity of the system makes it unlikely to be achieved through a single molecule. The speaker discusses their belief that metformin works by inhibiting complex one and triggering a homeostatic response. The speaker mentions the potential benefits and drawbacks of taking metformin, particularly in individuals who already lead healthy lifestyles. The conversation then shifts to discussing the potential therapeutic benefits of hypoxia, particularly in individuals with mitochondrial disorders. They describe their preclinical work in using hypoxia chambers to reduce oxygen delivery and improve ATP levels in mouse models.
The context discusses the role of mitochondria in energy transformations and the generation of ATP. The mitochondria can take in fats, carbohydrates, and proteins and break them down to harness electrons and create an electro-motive force. This electro-motive force can be used to generate an energy gradient that can be used to power various enzymes and processes in the cell. NADH and NAD+ are electron carriers that play a crucial role in this process. The decline in NAD levels and mitochondrial activity is associated with aging, and targeting the mitochondria may alleviate the decline in tissue function. The lab studies rare inborn errors of mitochondrial metabolism, which are typically single gene disorders that cause defects in the mitochondria at birth.
