How Old is Your Cellular Metabolism?

Where can we find the metabolic fountain of youth? Centuries are filled with an endless variety of magicians and now scientists searching for that magic potion to help us live forever. While I ultimately know that only heaven will be forever, present world research into the process of aging can lead to very beneficial therapies for our physical bodies and their dysfunctions. This article from Nature Scientific Reports suggests that the old paradigm of increasing genetic defects in our cell powerhouses, mitochondria, may not be the complete explanation for aging.

Scientists have long recognized that aging usually includes some degree of low energy and low cell growth. Obviously, the energy produces organelles, mitochondria, would be the prime suspects for dysfunction leading to such bodily dysfunction. Exactly how this happens or if this is the chicken or the egg remains unclear.

These researchers from the University of Tsukuba proposed and elucidate how epigenetic effects on SHMT2, serine hydroxymethyltransferase 2 plays a role in downregulating the mitochondria’s function. Lower expression (less SHMT2 protein produced by the gene) of SHMT2 was found in this mouse study to cause lower mitochondrial function. Apparently, lower SHMT2 function caused the liver cells in the mouse model to produce less taurine. Taurine is an amino acid that the mitochondria need for normal function.

While the accumulation of genetic defects in mitochondria does occur and may contribute, this research indicates metabolic control factors outside the mitochrondria play a role as well. This is an example of epigenetic control rather than genetic control. Genetic changes in DNA may cause the produced proteins to not function. This can cause cell death or dysfunction. However, epigenetic control occurs when the amount of that gene’s protein is produced at a higher or lower rate. It can also be when the produced protein remains active longer due to some modification of its breakdown. Epigenetics acts more as a knob turning a process up or down in degrees rather than on or off like a genetic mutation does.

There is good reason that epigenetics remains a hot topic in functional medicine. Researchers can easily discern that they are just scraping the surface of metabolic mechanisms which control our cell’s functioning. We as functional MD’s know that the research is both confirming our current practices AND leading to further ways we can help patients discern a path to healthier more abundant lives.

Original Article:
Haruna Tani, Takayuki Mito, Vidya Velagapudi, Kaori Ishikawa, Moe Umehara, Kazuto Nakada, Anu Suomalainen, Jun-Ichi Hayashi. Disruption of the mouse Shmt2 gene confers embryonic anaemia via foetal liver-specific metabolomic disorders. Scientific Reports, 2019; 9 (1) DOI: 10.1038/s41598-019-52372-6

Thanks to Science Daily:
University of Tsukuba. “Slowing down — Is aging caused by decreased cellular metabolism?.” ScienceDaily. ScienceDaily, 20 November 2019. <www.sciencedaily.com/releases/2019/11/191120131336.htm>.

Other articles on Cellular aging and SHMT2:
Wallace, D. C. Mitochondrial diseases in man and mouse. Science 283, 1482–1488 (1999).
Jacobs, H. T. The mitochondrial theory of aging: dead or alive? Aging Cell 2, 11–17 (2003).
Taylor, R. W. & Turnbull, D. M. Mitochondrial DNA mutations in human disease. Nature Rev. Genet. 6,
Trifunovic, A. et al. Premature ageing in mice expressing defective mitochondrial DNA polymerase. Nature 429, 417–423 (2004).
Kujoth, G. C. et al. Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging. Science 309, 481–484 (2005).
Khrapko, K. & Vija, J. Mitochondrial DNA mutations and aging: devils in the details? Trends Genet. 25, 91–98 (2008).
Bratic, A. & Larsson, N. G. The role of mitochondria in aging. J. Clin. Invest. 123, 951–957 (2013).
Ducker, G. S. & Rabinowitz, J. D. One-carbon metabolism in health and disease. Cell Metab. 25, 1–16 (2017).
Nikkanen, J. et al. Mitochondrial DNA replication defects disturb cellular dNTP pools and remodel one-carbon metabolism. Cell Metab. 23, 635–648 (2016).
Khan, N. A. et al. mTORC1 regulates mitochondrial integrated stress response and mitochondrial myopathy progression. Cell Metab. 26, 419–428 (2017).


Sanctuary Functional Medicine, under the direction of Dr Eric Potter, IFMCP MD, provides functional medicine services to Nashville, Middle Tennessee and beyond. We frequently treat patients from Kentucky, Alabama, Mississippi, Georgia, Ohio, Indiana, and more... offering the hope of healthier more abundant lives to those with chronic illness.

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