Just a quick post that suggests once again that metabolism is the key determinant of intelligence and brain size, not genetics. The study below demonstrated that mitochondria from different species can be cross-transplanted into cells from different species, and despite the vast differences in the genetic code of the nucleus of each species’ cells, the cells with the transplanted mitochondria were functioning normally. However, mitochondria from different species triggered different expression of genes in the cell nucleus and those gene expressions were mostly related to brain development. Thus, it may very well be possible to take a “lower” organism and endow it with superior intelligence simply by transplanting mitochondria from more intelligent species, including humans. Furthermore, it suggests that increasing intelligence in humans depends on increasing mitochondrial function (as well as number and size), and not by messing with the genetic code. Ray did mention this in several articles in regards to thyroid (T3) supplementation. Namely, even people with severe mental retardation were able to regain normal intelligence after chronic administration of T3. Conversely, people normally considered highly intelligent and even savants, behaved as if having mental retardation when their metabolic rate was lowered as a result of fasting, PUFA ingestion, infectious disease, etc.
http://www.sciencedirect.com/science/article/abs/pii/S0092867425005707
“…Next, using enforced mitophagy, the scientists created hPSCs devoid of human mitochondria and fused them to non-human primate PSCs, again creating cells carrying nuclear genomes from both species, but this time only non-human mitochondria. An analysis of composite cells containing either human or non-human mitochondria showed that the mitochondria were largely interchangeable despite millions of years of evolutionary separation, causing only subtle differences in gene expression within the composite nucleus. Interestingly, the genes that differed in activity among cells harboring human and non-human mitochondria were mostly linked to brain development or neurological diseases. This raises the possibility that mitochondria may play a role in the brain differences between humans and our closest primate relatives. However, Dr. Wu said, more research – especially studies comparing neurons made from these composite PSCs – will be needed to better understand these differences. Finally, the researchers studied how depleting mitochondria might affect development in whole organisms. They used a genetically encoded version of enforced mitophagy to reduce the amount of mitochondria in mouse embryos, then implanted them into surrogate mothers to develop. Embryos missing more than 65% of their mitochondria failed to implant in their surrogate’s uterus. However, those missing about a third of their mitochondria experienced delayed development, catching up to normal mitochondrial numbers and a typical developmental timeline by 12.5 days after fertilization.”
