Today, we're delving into mitochondrial dysfunction, a pivotal marker of chronic illness. This encompasses conditions like chronic fatigue often related to Chronic Inflammatory Response Syndrome from water-damaged buildings (CIRS-WDB) or mold exposure, Lyme disease, and candida overgrowth, among others. Furthermore, we'll explore a powerful combination that surpasses urolithin A in inducing mitophagy, alongside an intriguing peptide that addresses mitochondrial dysfunction.
To lay the groundwork for our discussion, it's crucial to comprehend what dysfunctional mitochondria entail, both on a grand scale and at the biochemical level. I've previously discussed mitochondria in various podcast episodes, focusing on broad overviews and the benefits of certain supplements and nutrients for mitochondrial health. However, with continuous advancements in research, today's post is dedicated to exploring new insights into potentially restoring function to dysfunctional mitochondria.
Mitochondrial dysfunction is often mentioned but understanding the root causes, such as genetic mutations, environmental stressors, toxins, and aging, is key. At the biochemical level, this dysfunction can involve issues in oxidative phosphorylation, increased reactive oxygen species (ROS) generation, disrupted calcium homeostasis etc..., and result in things like senescence or apoptosis, for example.
Oxidative phosphorylation, a vital metabolic pathway occurring within the inner mitochondrial membrane, is crucial for ATP production, the cell's energy currency. Dysfunction in this process, especially within the electron transport chain (ETC), can lead to severe consequences, including reduced ATP synthesis and increased ROS generation. For instance, aging and ROS accumulation contributes to mitochondrial DNA mutations.
And, given mtDNA's susceptibility to damage due to its proximity to the ROS-producing electron transport chain and its limited repair mechanisms, this leads to a detrimental cycle where mutations impair oxidative phosphorylation, reducing ATP production and increasing ROS generation, which in turn can further damage mtDNA.
Now, addressing mitochondrial dysfunction also involves considering nuclear DNA alterations and toxins (endogenous and exogenous), which can either exacerbate, contribute to, or initiate this damaging cycle. Various factors, including psychological stress, exposure to radiation and biotoxins, infectious agents, environmental pollutants, and nutrient deficiencies, can all contribute to mitochondrial dysfunction.
In terms of addressing this dysfunction, strategies include restoring function to existing mitochondria, removing damaged mitochondria through mitophagy, and promoting the generation of new, healthy mitochondria. Clinical trials have shown the effectiveness of supplements like L-carnitine, alpha-lipoic acid, CoQ10, membrane phospholipids, and NAD precursors in supporting mitochondrial function.
Regarding mitophagy, urolithin A has gained attention. Though, a recent study actually showed how urolithin A is more effective when combined with EGCG in particular. This combination was used in a study conducted on mice, and the researchers were looking at the brain (Alzheimer's disease, specifically). And, they found a drastic difference when stacking the two compounds when it came down to mitigating mitochondrial dysfunction and inducing mitophagy in AD.
For mitochondrial biogenesis, compounds like PQQ, resveratrol, EGCG, and specific peptides such as SS-31 have shown potential.
SS-31, in particular, merits further discussion due to its ability to bind to cardiolipin, thus supporting more efficient oxidative phosphorylation (better ATP yields with lower ROS generation) and possibly helping to "fix" or support dysfunctional mitochondria themselves.
I will be doing further deep dives into SS-31 peptide. Stay tuned.
*Always only ever work with a medical professional.
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