It has been shown that, with age, mitochondrial function decreases or worsens in different tissues.

This implies an accumulation of morphological alterations at the level of the mitochondria and, in addition, a decrease in the respiratory capacity of these organelles.

Mitochondrial metabolism is essential for maintaining proper cellular function. In fact, several diseases associated with aging, such as neurodegeneration and diabetes, are related to alterations in the function of mitochondria.

Dr. Moisés De Vicente – Neolife Medical Team

Recent studies have shown that the inability to get rid of cell-damaged mitochondria plays a crucial role.

The aging process is closely related to the functional decline of our mitochondria. Since Professor Harman described the theory of mitochondrial free radicals (1) in 1956, this relationship has been established and accepted in a large sector of the scientific community.

It is true that the intrinsic mechanism, the final key, the last link through which this process takes place, is still unknown. What is clear is that mitochondrial metabolism is essential for preserving proper cell function. In fact, several diseases associated with aging, such as neurodegeneration and diabetes, are related to alterations in the function of mitochondria. Specifically it seems that it is the accumulation of mitochondria, “malfunctioning” so to speak, that clearly predisposes us to the first alterations of the cellular metabolism that leads to the onset of aging (2).

It has been shown that, with age, mitochondrial function decreases or worsens in different tissues. This implies an accumulation of morphological alterations at the level of the mitochondria and, in addition, a decrease in the respiratory capacity of these organelles (3). However, the difficult thing is establishing which came first, the chicken or the egg. Are these changes the precursors of cellular aging? Or are these changes the result of aging that has already begun? We could even consider that these changes are nothing more than adaptive movements of the mitochondria to balance certain disruptions already established by age.

It seems that the accumulation of mutations in mitochondrial DNA and its inability of to regenerate are the main factors involved in loss of functionality (4). Furthermore, recent studies have shown that the inability to get rid of cell-damaged mitochondria, also known as mitophagy, plays a crucial role (5). This functional alteration is characterized by a decrease in oxygen consumption, which implies a decrease in the genesis of ATP, decreases the membrane potential, increases the production of free radicals and decreases the levels of coenzyme Q10. The result of all this is a decrease in glucose and pyruvate at the intracellular level and the oxidation of fatty acids (6).

Therefore, it is mitochondrial metabolism and mitochondrial divisions and fusions that seem to hold the key to regulating mitochondrial function and mitochondrial quality, inducing mitophagy and stabilizing the mutations that could occur in mitochondrial DNA (7). Based on this, alterations in this metabolism and these processes, for whatever reason they occur, are the prelude to ageing.

The question is clear. So how can I improve my metabolism and mitochondrial functionality? At Neolife, we believe it would be ideal to be able to measure this metabolism in order to provide each of our patients with a series of measures and supplements to optimize their mitochondria to the fullest. However, this is not currently feasible. If we could measure intracellular and mitochondrial oxidative stress we would be able to evaluate this functionality indirectly.

In any case, it seems essential to be able to help our mitochondria, even blindly. Several studies have been published with molecules that are capable of obtaining excellent results in this regard. Obviously, the coenzyme Q10 is one of them, as we have mentioned in previous articles. Likewise, melatonin has a certain capacity to optimize this metabolism (the truth is that at high doses melatonin optimizes countless processes in our body) by reducing the production of free radicals, which brings about a reduction in oxidative stress (8).

Other molecules that improve cellular activity are acetyl L carnitine, phosphatidylserine and vitamin B3. Specifically, acetyl L carnitine plays an important role in mitochondrial intermediary metabolism, facilitating the elimination of free radicals produced during beta-oxidation. Thanks to this, it possesses an antioxidant and antiapoptotic (avoids cell death) capacity with inflammatory, analgesic and neuroprotective properties (9).

BIBLIOGRAPHY

(1) Harman, D. Aging: a theory based on free radical and radiation chemistry. J. Gerontol. July 1956, Vol. 11, 298–300.

(2) David Sebastián et al. Mitochondrial Dynamics: Coupling Mitochondrial Fitness with Healthy Aging. Trends in Molecular Medicine, March 2017, Vol. 23, No. 3.

(3) Lopez-Otin, C. et al. The hallmarks of aging. Cell. 2013, Vol. 153, 1194–1217.

(4) Kujoth, G.C. et al. Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging. Science. 2005, Vol. 309, 481–484.

(5) Palikaras, K. et al. Coordination of mitophagy and mitochondrial biogenesis during ageing in C. elegans. Nature. 2015, Vol. 521, 525–528.

(6) Mourier, A. et al. Mitofusin 2 is required to maintain mitochondrial coenzyme Q levels. J. Cell. Biol. 2015, Vol. 208, 429–442.

(7) Chan, D.C. Fusion and fission: interlinked processes critical for mitochondrial health. Annu. Rev. Genet. 2012. Vol. 46, 265–287.

(8) Russel J. Reiter et al. Mitochondria: Central Organelles for Melatonin′s Antioxidant and Anti-Aging Actions. Molecules. 2018, Vol. 23, 509.

(9) Giovanna Traina. The neurobiology of acetyl-L-carnitine. Frontiers in Bioscience, Landmark, 21, 1314-1329, June 1, 2016.