Yet another study demonstrating the key role metabolism plays in aspects of health firmly considered by medicine to be completely non-metabolic in nature. It has been conclusively shown that as humans age, not only do they experience chronically elevated inflammatory states, but those states exacerbate with advancing age. In others words, not only do we break down with aging, but the rate of the breakdown accelerates as we age. Chronic inflammation is now recognized as perhaps THE main causal factor in virtually all chronic diseases known to medicine, and especially the top “killers” such as heart disease (CVD), cancer, diabetes, neurological disorders, liver disease, and bone degradation. Despite this knowledge, medicine still shies away from recommending that people take anti-inflammatory remedies (such as aspirin) on a regular basis. If anything, medicine has been engaged in a relentless smearing and fear-mongering campaign against aspirin, trying to convince the public that aspirin is so “dangerous” that even people with established CVD should only consider aspirin after all other options have been exhausted. Btw, multiple studies have demonstrated that aspirin’s benefits against chronic diseases (not just CVD) cannot be explained solely by its anti-inflammatory effects since other so-called NSAID do not have the same benefits as aspirin, and some of them even increase risk of CVD and other conditions. The study below may offer a clue in regards to the “mysterious” benefits of aspirin. Namely, the study demonstrates that the majority of chronic inflammation seen with aging is driven by declining mitochondrial function, and and that restoring said function ameliorates (or even stops) the inflammatory process. It just so happens that aspirin is unique among the widely used NSAID in that it is very pro-metabolic, increasing the entire metabolic cascade, from glycolysis to the electron transport chain (ETC). In addition, aspirin has also been shown to increase the number and size of mitochondria inside cells. Other pro-metabolic substances such as progesterone, thyroid, DHEA, etc would probably have similar effects in mitochondria and inflammation, and this has already been confirmed in multiple studies, including human ones. So, once again, we discover that something as pervasive, important and “incurable” is nothing but a symptom of metabolic dysfunction, that may be easily addressable with cheap and widely available remedies.
Oh, and last but not least, the study below focused mostly on ovarian failure seen in menopause and beyond. In other words, menopause itself is likely nothing but a symptom of the chronic inflammation, driven by mitochondrial dysfunction. As such, menopause may be reversible by the same simple pro-metabolic measures mentioned above. Ray mentioned quite a few cases of women in their 50s and eve 60s conceiving children after using progesterone for a few months. I would go out on a limb here and suggest that progesterone is even more effective when combined with DHEA and this fact has already been confirmed in human studies. Adding aspirin and/or thyroid may lead to a state of society where some of a women’s grandchildren may be older than their children:-)
https://doi.org/10.1186/s12967-025-06966-6
“…As women age, the decline of ovarian function is both natural and inevitable. However, the mechanisms underpinning this aging process have remained somewhat enigmatic. Ju and colleagues propose that inflammation initiated by mitochondrial dysfunction is a significant catalyst for this decline. They argue that mitochondrial health is not merely a bystander in the aging process but rather a critical determinant that can either exacerbate or mitigate ovarian aging.”
“…The researchers conducted a series of experiments that illuminated the nexus between mitochondrial dysfunction and inflammation in ovarian tissues. Their findings suggest that as mitochondrial activity declines, there is a concomitant increase in pro-inflammatory cytokines, which are signaling molecules that can amplify the inflammatory response. This inflammatory milieu can induce a cascade of detrimental effects on ovarian cells, thereby accelerating their aging process. In their study, the authors meticulously present data showing elevated levels of inflammatory markers in aged ovarian tissues. These findings were complemented by analyses of mitochondrial morphology and function, which demonstrated a striking loss of mitochondrial integrity in tissues from older subjects. The correlation between compromised mitochondrial function and heightened inflammatory responses was compelling, suggesting that targeting mitochondrial health could offer new avenues for therapeutic intervention.”
