What is mitochondrial disease? Most mitochondrial function and biogenesis is controlled by nuclear DNA. Human mitochondrial DNA encodes only 13 proteins of the respiratory chain, while most of the estimated 1,500 proteins and components targeted to mitochondria are nuclear-encoded. Defects in nuclear-encoded mitochondrial genes are associated with hundreds of clinical disease phenotypes including anemia, dementia, hypertension, lymphoma, retinopathy, seizures, and neurodevelopmental disorders.
Spindle transfer, where the nuclear DNA is transferred to another healthy egg cell leaving the defective mitochondrial DNA behind, is a potential treatment procedure that has been successfully carried out on monkeys. Using a similar pronuclear transfer technique, researchers at Newcastle University successfully transplanted healthy DNA in human eggs from women with mitochondrial disease into the eggs of women donors who were unaffected. In September 2012 a public consultation was launched in the UK to explore the ethical issues involved. Human genetic engineering is already being used on a small scale to allow infertile women with genetic defects in their mitochondria to have children. On 26 June 2013, the United Kingdom government agreed to legalize the three-person IVF procedure as a treatment to fix or eliminate mitochondrial diseases that are passed on from mother to child. The procedure could be offered within two years once regulations are established.
There are a host of other cardiovascular disease states, more particular to the heart, that result from a shift from a CR/LE pathway driven to CG/CM pathway driven status. Inflammation, ROS and glycation are neuropathic and can disrupt the cardiac cycle, leading to arrhythmias, fobrillation and infarction, as well as causing valvular and endocardial lining damage. Mitochondrial inefficiency and low mitochondrial numbers can reduce ATP production and force of contraction, as found in congestive heart failure and ventricular hypertrophy. Shifting the drive state from CG/CM to CR/LE has been shown to be neuroprotective, as well as neuroregenerative in both heart disease and diabetic neuropathy. This metabolic shift has been shown to increase mitochondrial numbers in both cardiac and skeletal muscle, to increase ATP production and to increase muscular force of contraction, thus relieving all the above mentioned conditions. Our three gold medal winners perform all these functions, in addition to their anti-diabetic and anti-cancer functions, as described earlier. The silver medalists synergistically support the gold medalists. Finally, we are ready to discuss our selected dietary supplements.
As we saw from the previous section, the glycolytic and mitochondrial metabolic pathways form a catabolic core system driven by CG and CR. Furthermore, these systems make coherent and consistent requisite changes depending on the cell state in all animal organisms and all of their cell types. No matter what the status of myriad regulatory elements superimposed on the ancient core system, it must respond in a flexibly limited fixed manner, or the global system collapses. Apoptosis and novel cancer therapies show some of the bounds of this limited flexibility. In normal cells, the core system can toggle back and forth between the CG and CR states. It cannot do this, either easily, or at all, in the cancer cell, as a result of mutations in the core system or in the regulatory elements of the core system. We distinguish this mutationaly â€~stuck' cancerous growth state from the normal CG state by referring to it as the cancer metabotype, or CM, for short. It has long been felt that the core system was a mere normal handmaiden to cell growth factors and other regulatory elements, and therefore, unworthy for investigation as a means of chemotherapeutic attack. (The sad tale of this 54 year drought can be search engined under Bambeck cancer: Mainstream Science Dogma Reversal, on the internet.) Recent developments show that many types of cancer cells can be growth arrested, killed or even differentiated by direct attack on the core system, its most intimate regulators or nearest neighbor/function partners. However, cancer cell kill therapies are neither the thrust, nor the scope of this paper, albeit the logic behind such therapies is well within its purview. Our primary focus is to define the basic CG/CM and LE/CR systems and to conduct a search for phytonutrient regulators which rectify the system in a way that helps to prevent or renormalize the three major diseases of aging, and which promote life extension. Thus, we will give a cursory overview of cancer in terms of our metabolic flow chart, and some of the therapeutic logic that can impact cancer.