An hour-long discussion of how mitochondrial dysfunction can result in various chronic diseases, and how the assumption that an anatomical division of disease is a driving assumption for how medicine is organized, and how that may block correct description and diagnosis of disease.
The speaker is Douglas C. Wallace, Ph.D.; Director, Center for Mitochondrial and Epigenomic Medicine (CMEM); Professor, Department of Pathology & Laboratory Medicine, The Children's Hospital of Philadelphia.
He does an especially good job of describing how malfunction in a single organelle can cause various diseases in various seemingly unrelated organs.
Some useful quotes below the video:
"Our hypothesis (that we've been testing for the last 45 years) is that bioenergetic dysfunction lies at the nexus of the genetic and environmental "causes"; and that the "common-complex" diseases are bioenergetic diseases, and not anatomical diseases." 7:07.
"Now each cell has hundreds of thousands of these mitochondrial DNAs, and they're constantly replicating inside your cells right now. And if you doubt that they're active and vital in there, talking to each other; tonight when it's very very quiet and your spouse is not snoring if you just concentrate you'll feel them wiggling in there." 16:49Discussing cells with different mitochondrial genotypes from mutation and division:
"Some with good mitochondrial DNAs and high energy, some with bad mitochondrial DNAs and low energy, and if it's below the minimum energy for that tissue, then you will get a phenotype. The equivalent of a biological, a metropolitan brownout. So if there was a line voltage decline in LA, all the electrical systems wouldn't fail at one time. The first thing that would go would be the fluorescent light bulbs, then certain elevators, then certain electrical motors, but the incandescent light bulbs would just get dimmer and dimmer.
"Well the same is true for your body. Different parts of your body rely on energy to different extents, so as the energy declines, you're going to get organ-specific symptoms of a systemic defect." 17:35Noting the wild variation in expression between mitochondrial defects:
"If you inherit that from your mother you're fine until midlife, and then you'll lose your hearing (sensory-neural hearing loss). But if you get treated by aminoglycoside antibiotics, you'll go deaf within a week. OK? Mutation in the tRNA leucine gene, another protein synthesis mutation at 3243; at 30 % mutant will give you diabetes, 50% mutant give your neuromuscular disease, 100% mutant and you are dead." 18:55He goes on with many more examples.
"So we have a quantitative genetics with totally different clinical phenotypes." 20:15
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| Tissue-specific Symptomatology |
"So why would there be tissue-specific symptomatology? Well because different tissues rely on mitochondrial energy for different extents [sic]... [Examples] ...So in fact when you think energetically, much of anatomy is about energetics, not anatomy." 21:12
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| "The take-home lesson" |
"If the, in fact, the cells are sick, they cannot undergo apoptosis, then the mitochondria are released into the bloodstream, and they are perfectly good bacteria, and you're going to get inflammation. And that's why we believe all of these diseases have an inflammatory component." 23:54
He doesn't discuss my favorite topic, the impact of omega-6 fats on mitochondria and therefore health, but it fits nicely with his hypothesis. For instance, the part of mitochondria that causes the immune reaction and inflammation he describes is cardiolipin released with oxidized linoleic acid into the blood stream. [2]
Do watch the whole thing!
1.
A Mitochondrial Etiology of Common Complex Diseases. UCLA CTSI; 2017. https://www.youtube.com/watch?v=1aCHrHwm_AI. Accessed December 20, 2019.
2. Tuominen Anu, Miller Yury I., Hansen Lotte F., Kesäniemi Y. Antero, Witztum Joseph L., Hörkkö Sohvi. A Natural Antibody to Oxidized Cardiolipin Binds to Oxidized Low-Density Lipoprotein, Apoptotic Cells, and Atherosclerotic Lesions. Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26(9):2096-2102. doi:10.1161/01.ATV.0000233333.07991.4a
Hey Tucker,
ReplyDeleteGreat summary. I wrote down the slides and key points when I watched it circa July 2018 into this Google Doc. Thought you might get some use out of it for reference.
That's terrific! Thanks!
Delete