Chapter 7. Mitochondrial Function
In order for the human body to function, it needs a constant and correct supply of energy.The entire process of obtaining energy from foods initially consumed is called energy metabolism, and the biochemical reactions of this exchange occur in special cell organelles - mitochondria.
Mitochondria are present in every cell, but depending on the needs of the organ, their number can vary significantly.The most demanding areas in terms of energy are the heart, muscles and brain.
The uniqueness of mitochondria lies in the fact that they are not completely homogeneous with the rest of the organelles (parts) of the human cell; their origin is significantly different.At the dawn of the evolutionary process, the mitochondrion was a separately living bacterium - an alpha-proteobacterium, the peculiarity of which was the ability to profitably consume oxygen.At that time, the production and use of oxygen was unusual for microorganisms, and the interaction of cyanobacteria (which could produce O
Proteins, fats, carbohydrates - all substances entering the human body must be converted into special molecules in which energy is “conserved”.These molecules are adenosine triphosphoric acid (ATP) molecules.They are the universal energy currency for any cell and any organ.The mitochondrial pool is not a homogeneous composition of organelles identical throughout the human body, but a rather heterogeneous group.Mitochondria can vary significantly in their energy potential.
If the processes of synthesis of these molecules are disrupted at one stage or another, a deficiency in the supply of energy and heat to the cell develops, and it, therefore, loses the ability to function normally.Cells that are not properly provided with energy suffer and reduce their activity, and in a critical case, go into apoptosis - the process of programmed cell death.This is how mitochondrial pathology and associated organ dysfunction develop.
Just 15–20 years ago, mitochondrial pathology was considered exclusively as a narrow area of extremely rare (orphan) genetic diseases, which, with the exception of specialized specialists, even an experienced clinician may never encounter in their practice.However, over time, the concept of “mitochondrial dysfunction” and “mitochondrial pathology” have become one of the obligate, that is, mandatory, components of many systemic diseases.
If a person has a “bad”, functionally reduced pool of mitochondria, then first of all, as noted earlier, a number of organs that require a large amount of energy will suffer.A decrease in the activity of the mitochondrial pool in the central nervous system will lead to a decrease in cognitive abilities - memory, low learning ability and rapid exhaustion.Disruption of energy metabolism in cardiomyocytes, the cells of the heart, will lead to a condition called cardiomyopathy;in skeletal muscles – to muscle weakness, fatigue, slower development of motor skills;in the liver - to disruption of the entire functionality of detoxification mechanisms, and in the endocrine glands - to disruption of the synthesis of hormones that control the activity of organs and systems.This is how one of the central vicious circles is formed - hormonal and mitochondrial dysfunction, which mutually aggravate each other.
Hormonal and mitochondrial functions can be considered supersystems for the whole organism, since their functional activity ensures the routine and coordinated functioning of organs and systems.
Mitochondrial dysfunction, metabolic syndrome and generational degeneration
Mitochondrial dysfunction underlies classical systemic diseases, including the metabolic syndrome already mentioned several times in the book.According to a number of modern studies, diabetes and obesity are directly related to mitochondrial dysfunction.The accumulation of mutations and damage to mitochondrial DNA, due to inflammatory processes and increased production of reactive oxygen species (ROS), which due to the duration of pathological processes is not compensated by antioxidant systems, leads to systemic hormonal and enzyme failure.In turn, the accumulation of “errors” in mitochondrial genetic material over time aggravates the course of metabolic syndrome.The accumulation of such errors does not lead to the development of an oncological process, as with the accumulation of mutations in the genetic material of the cell itself, but it disrupts the entire energy metabolism as a whole.
Thus, mitochondrial dysfunction underlies the development of metabolic syndrome and develops as a result of it, closing a vicious circle.
It should be noted that the development of mitochondrial dysfunction is exactly the point of no return, where acute inflammation develops into chronic inflammation, and from chronic inflammation into autoimmune pathology, followed by the risks of developing cancer and degeneration.
One mechanism of generational degeneration in general is the accumulation of epigenetic changes that occur from generation to generation.That is, those certain harmful factors that began to develop and accumulate in our grandmothers, processes of methylation disorders, metabolic syndromes, the volume of exogenous intoxicants that we listed in previous chapters, lead to inevitable epigenetic changes in DNA.Epigenetic changes differ from genetic ones in that the structure of one’s own DNA does not change, but some of its zones become inactive.In the next generation, new changes are added to the epigenetic changes that the grandmother passed on to her child.
The intensity of the accumulation of epigenetic and mitochondrial errors in our time is significantly increasing due to a decrease in compensatory capabilities, on the one hand, and a significantly increasing total load, on the other.The critical accumulation of mitochondrial and associated hormonal pathology leads to an increase in the number of infertile couples, miscarriages, and an increase in the number of children born who are weakened, low-weight, premature, very poorly adapted to environmental conditions, and have weak potential, which is absolutely insufficient to withstand the stress that great-grandmothers and grandmothers endured without much change when they were children.
Mitochondrial dysfunction and cancer
According to current scientific research, cancer can develop due to various reasons, both genetic and as a result of long-term metabolic disorders.A cancer cell, like a healthy cell, has its own mitochondria, but their functional activity differs significantly.The mitochondria of a cancer cell are not aimed at creating energy compounds; the processes of oxidation and reduction in them are disrupted, resulting in the production of excess amounts of reactive oxygen species (ROS).
Not all reactive oxygen species are absolute evil; in specialized cells of the immune system they become an active factor against foreign agents (for example, in phagocytes).However, somatic cells are not adapted to deactivate large amounts of ROS, so they are inevitably damaged, including their DNA, which leads to changes in genetic information and activation of the oncological process.Thus, mitochondrial dysfunction itself can provoke the development of an oncological process.Mutated dysfunctional mitochondria lead the cancer cell to change energy metabolism; the cell no longer needs to constantly receive oxygen, like a normal one; it uses glucose directly as a substrate to obtain energy through the process of anaerobic (i.e., oxygen-free) oxidation.Thus, the malignant cell begins to be able not only to survive, but also to reproduce under hypoxic conditions.From the above, two extremely important conclusions follow: mitochondrial function must be taken into account in the pathogenesis and development of malignant neoplasms, and a patient with an oncological process must be transferred to a strict elimination diet with the exclusion of carbohydrate load and the body switching to the consumption of ketones as the main source of energy.
Mitochondrial dysfunction and aging
The accumulation of mutations in mitochondrial genetic information is associated not only with the development of severe systemic diseases, but also with the development of aging in general.Dysfunctionality of the mitochondrial pool inevitably leads to a decrease in the performance of organs and systems, and the accumulation of genetic mutations associatedly increases the risk of developing oncological processes with age.
With age, catabolism processes, that is, decay processes, including for the purpose of obtaining energy, in the human body begin to prevail over synthesis processes (anabolism).Strengthening and acceleration of decay processes occurs as a result of hormonal depletion (it is hormones that trigger synthesis processes, which is why some of them are commonly called “anabolic steroids”), against the background of a chronic inflammatory process, as well as as a result of depletion of the overall compensatory potential, which includes antioxidant systems.
Partly by correcting mitochondrial status by replenishing antioxidants, the anti-aging effect of many drips and procedures that are fashionable these days is achieved.However, blindly increasing antioxidants in order to suppress oxidative processes in the body is a futile and even unsafe path in anti-aging therapy.
Correction of the mitochondrial pool is a complex and complex task, which includes both leveling “defective” mitochondria and stimulating the regeneration of functionally active mitochondria, and not only and not so much replenishing the deficiency of cofactors, vitamins and antioxidants, which is what modern nutrition and preventive medicine do.
Mitochondrial therapy and the regeneration stage in the treatment of patients with systemic diseases
According to the concept we developed, recovery must go through three mandatory stages: antigenic unloading, detoxification and regeneration, for which mitochondrial and hormonal support are mandatory and constant components.
It is worth noting that just ten years ago, it was enough for our patients to introduce an elimination diet and antigen unloading with a little support from detoxification systems to obtain a sustainable positive treatment result.That is, our treatment previously could really be limited to eliminating what is “unnecessary” for the body, and then the patient got out on his own and no longer needed help.
Modern patients have extremely low intrinsic regenerative potential; their basic condition should be defined as total immunomitochondrial diathesis.Their treatment cannot be limited to elimination; it must include all the components of the “health pyramid” and the obligatory regenerative stage, which is aimed not only at restoring functions lost during the disease, but also at preventing repeated regressions.
Repeated regressions of patients with immunomitochondrial syndrome are not as deep and severe as the first ones they encountered (such as, for example, a total rollback of acquired skills in regressive autism after an infection and/or polyvaccination load).Nevertheless, the “return” of at least part of the complaints means the need to conduct treatment again, often more intensively and using more aggressive methods of therapy.
It was the desire to “let go” of the patient, so that he would not return and no longer need therapeutic interventions, that became the basis for the development of the regenerative rehabilitation stage, which is the subject of the final chapter.