PQQ Effects on Cell Growth and New Mitochondria
Mitochondria can produce damaging reactive oxygen species (ROS) as a by-product of normal function. Over time, ROS degrade mitochondrial DNA (mtDNA), interfering with cellular energy production. When a cell loses mitochondria, eventually apoptosis or cell death can occur. Most cell’s strategy for dealing with damage is to “recycle” or turnover mitochondria on a regular basis.
Mitochondria replicate more often than the cells in which they live. In small animals, this occurs between one and a half to three days in liver cells, and two to four weeks in mature brain cells. Generally, the faster the mitochondria turn over, the better. In other words, it is better to replace mitochondria before too much mtDNA damage accumulates. Regarding turnover, the best data science has is related to caloric restriction. Studies have shown that calorie restriction speeds mitochondrial turnover (e.g., if calories are not used, less need fo mitochondria). In contrast, exercise slows mitochondrial turnover and appears to promote mitochondriogenesis. Appreciate, however, that these changes are not huge. A change as little as 5 to15 percent can be dramatic from a normal energy perspective.
So what are the effects from PQQ supplementation and withdrawal?
The only data that we have are from animal studies. Giving rats a supplement of pyrroloquinoline quinone that were previously fed diets devoid of PQQ, increases muscle and liver mitochondria about 10 to 20 percent somewhere between half a day to one and a half days. In contrast, methoxatin depletion causes reversal and multiple gene changes in about one to two days.
With regard to humans, there are ways of scaling data from rats to humans. Using those procedures, our best guess is that the withdrawal response in humans from a typical pyrroloquinoline quinone supplement (e.g., 10 milligrams) is somewhat rapid, probably within a week. Assuming circumstances short of starvation, the mitochondrial amounts will return to their relative basal levels. We need to clarify this as “relative basal levels” because the level may depend on the degree to which the respective person is exercising or taking other mitochondria stimulating substances.