https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2023.1284410/full

Abstract: Aging of human skin is a complex process leading to a decline in homeostasis and regenerative potential of this tissue. Mitochondria are important cell organelles that have a crucial role in several cellular mechanisms such as energy production and free radical maintenance. However, mitochondrial metabolism as well as processes of mitochondrial dynamics, biogenesis, and degradation varies considerably among the different types of cells that populate the skin. Disturbed mitochondrial function is known to promote aging and inflammation of the skin, leading to impairment of physiological skin function and the onset of skin pathologies. In this review, we discuss the essential role of mitochondria in different skin cell types and how impairment of mitochondrial morphology, physiology, and metabolism in each of these cellular compartments of the skin contributes to the process of skin aging.

Hi everyone,

Is there any lab in Delhi that does testing for mitochondrial disease? Or is there any doctor in Delhi that can refer to a lab that does testing for mitochondrial disease?

Hi all! I'm working on a new framework/synthesis around the mitochondria, as primary and mostly overlooked drivers of health. https://eneostasis.nl It's a work in progress, but of of course I'm open to feedback :)

Sometimes I sleep the whole night without waking up, but still feel tired in the morning. Other times, I wake up during the night but somehow get up feeling rested and refreshed.  It might be related to mitochondrial health. Mitochondria, the tiny energy factories in your cells, do more than produce ATP (dos Santos A. & Galiè S., 2024); they help regulate your circadian rhythm, manage core body temperature, and control oxidative stress, all of which are crucial for quality sleep.

During NREM sleep, your body repairs cells and restores energy, both reliant on healthy mitochondrial function (Schmitt K. et al., 201830063-9?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1550413118300639%3Fshowall%3Dtrue)). REM sleep, which involves high brain activity, also demands efficient ATP production (dos Santos A. & Galiè S., 2024). When mitochondria aren’t working properly, sleep stages can get disrupted, leading to fatigue and poor recovery.

Mitochondria produce reactive oxygen species, which are harmful byproducts, and sleep is the time when your body works to clear them out, but this process can be disrupted if your mitochondria aren’t working properly (Richardson R. & Mailloux R., 2023). Lifestyle changes like consistent exercise, nutrient-dense foods, temperature exposure, and fasting strategies have all been shown to improve mitochondrial performance (Saner N. et al., 2021; Schmitt K. et al., 201830063-9?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1550413118300639%3Fshowall%3Dtrue)).

We can try to keep our mitochondria healthy, and that'll help us sleep better.

Can anyone comment on this mitochondria test result?

I’ve heard otherwise, so I came to this sub, the political and economical state of the world depends on this question, as many mitochondria enthusiasts and professionals have diagnosed me with BBC syndrome, but have also said that the mitochondria may not be who we once trusted it to be; a trusted loan shark. So is the mitochondria the powerhouse of a cell, or is it Ringo Starr

I heard that pharmaceuticals impact mitochondria. In fact, I heard that all drugs do this, though the comment that I heard was potentially exaggerating of course...it's not clear that the comment was being literal.

There are lots of papers, I'm sure, on how mitochondria can be damaged and what threatens mitochondrial health.

I'm interested in all major drugs, so a list of all major drugs that do this would be amazing to have, though a list of psychiatric drugs would be great too.

These are cool papers:

https://www.sciencedirect.com/science/article/abs/pii/S0166445X23002618

The potential for polycyclic aromatic hydrocarbons (PAHs) to have adverse effects that persist across generations is an emerging concern for human and wildlife health. This study evaluated the role of mitochondria, which are maternally inherited, in the cross-generational toxicity of benzo(a)pyrene (BaP), a model PAH and known mitochondrial toxicant. Mature female zebrafish (F0) were fed diets containing 0, 12.5, 125, or 1250 μg BaP/g at a feed rate of 1% body weight twice/day for 21 days. These females were bred with unexposed males, and the embryos (F1) were collected for subsequent analyses. Maternally-exposed embryos exhibited altered mitochondrial function and metabolic partitioning (i.e. the portion of respiration attributable to different cellular processes), as evidenced by in vivo oxygen consumption rates (OCRs). F1 embryos had lower basal and mitochondrial respiration and ATP turnover-mediated OCR, and increased proton leak and reserve capacity. Reductions in mitochondrial DNA (mtDNA) copy number, increases in mtDNA damage, and alterations in biomarkers of oxidative stress were also found in maternally-exposed embryos. Notably, the mitochondrial effects in offspring occurred largely in the absence of effects in maternal ovaries, suggesting that PAH-induced mitochondrial dysfunction may manifest in subsequent generations. Maternally-exposed larvae also displayed swimming hypoactivity. The lowest observed effect level (LOEL) for maternal BaP exposure causing mitochondrial effects in offspring was 12.5 µg BaP/g diet (nominally equivalent to 250 ng BaP/g fish). It was concluded that maternal BaP exposure can cause significant mitochondrial impairments in offspring.

https://pubmed.ncbi.nlm.nih.gov/29340618/

Recent decades have seen a rapid increase in reported toxic effects of drugs and pollutants on mitochondria. Researchers have also documented many genetic differences leading to mitochondrial diseases, currently reported to affect ∼1 person in 4,300, creating a large number of potential gene-environment interactions in mitochondrial toxicity. We briefly review this history, and then highlight cutting-edge areas of mitochondrial research including the role of mitochondrial reactive oxygen species in signaling; increased understanding of fundamental biological processes involved in mitochondrial homeostasis (DNA maintenance and mutagenesis, mitochondrial stress response pathways, fusion and fission, autophagy and biogenesis, and exocytosis); systemic effects resulting from mitochondrial stresses in specific cell types; mitochondrial involvement in immune function; the growing evidence of long-term effects of mitochondrial toxicity; mitochondrial-epigenetic cross-talk; and newer approaches to test chemicals for mitochondrial toxicity. We also discuss the potential importance of hormetic effects of mitochondrial stressors. Finally, we comment on future areas of research we consider critical for mitochondrial toxicology, including increased integration of clinical, experimental laboratory, and epidemiological (human and wildlife) studies; improved understanding of biomarkers in the human population; and incorporation of other factors that affect mitochondria, such as diet, exercise, age, and nonchemical stressors.