The complexity of the human species and our potential for awareness requires a certain perfect precision in our material make-up which we ourselves may not yet be fully cognizant of. Life uses energy to self-organize toward ever-greater energy, synergy and complexity. Life’s evolutionary building of energy and greater order is in a sense the opposite of chaos and entropy. Through anthropogenic eyes we can see that hominids started traveling down the route towards metabolic energy crisis, chaos and disorder when cereal agriculture shifted our essential fatty acid consumption more toward Omega-6 dominance at the expense of Omega-3. The 10,000 years of cereal consumption and consequent breakdown in our cellular energy generation lowers the moral and spiritual consciousness of the species, allowing all manner of violent, criminal, predatory, parasitic, tyrannical and anti-life thought, behavior and processes to occur.
In exploring Borg Metabolic X syndrome I went looking for why there is a decline in oxy phos ATP generation and consequent reliance on aerobic and anaerobic glycolysis to generate ATP. When fats are heated, hydrogenated, made into transfats or when omega-6 from cereals is eaten in excess of omega-3 this destroys the structure and function of the cell membranes and mitochondrial membranes. When these misshapen fats are incorporated into the cell membrane it becomes saturated, rigid, less flexible and unable to function properly. This in combination with the free radicals from chronic stress, industrial food, toxins, pollution leads to systemic cellular inflammation, insulin resistance and the breakdown of the intake mechanisms for getting both glucose into the cell and pyruvate into the mitochondria.
When cell voltage falls as a consequence of inadequate ATP production this throws off active ATP dependent transport, uptake receptors, membrane potential, function of ion gates (channels), pH differentials, nutrition and detoxification of the cell, and reduces the energy available for cell maintenance and repair. As the cell loses its metabolic intelligence the organism experiences an associated loss of consciousness, communication and sentience, whereby it falls out of bliss connection with Gaia and descends into an ever-deepening depleted or “needy” state.
Besides all the other factors in biological systems decline that leads to the fallen Borg condition, we must focus intently on the decreased quality of fatty acids and their disproportion in the diet as being instrumental to species degeneration; because of the consequent loss of Cardiolipin (L4CL) in the inner membrane of the mitochondria interferes with pyruvate uptake leading to the decline in oxy phos ATP generation. Vibrant cellular mitochondria respiration is the basis for good health. Depending on their energy demand organs are affected to differing degrees by impaired of mitochondrial function; the heart, the skeletal muscle cells, the brain and retina therefore show a much more pronounced response to mitochondrial insufficiency.
Thus we can say that Borg Metabolic X and its associated energy decline has a lot to do with cardiolipin loss in the inner membrane of the mitochondria. Insufficiency of this vital component and the reduced ATP underlie all degenerative disease and the mental-emotional-social decline of the species into undifferentiated “closed” Borg consciousness. The humanization process of specificity, complexity, depth, integration and “openness” are reduced due to this energy slump...even as human culture itself slowly evolves and technological progress powers ahead. The veneer of civilization thus props up the underlying metabolic-spiritual decline of the species, even as it is falling apart at its power-generating source. This loss of energy is ultimately dehumanizing both of the individual body, mind and soul, but also greatly undermines the overall progress of human evolution itself.
The symptoms of the Borg Metabolic X syndrome include: demineralization, HPA-hyperactivation, burnt-out adrenals, reduced thyroid, increased insulin resistance and collapsed mitochondria energy generation. This crippled condition forms the basis to the spiritual castration of populations into the uncreative slave populations (the sleep of sheep). It doesn’t take much imagination to see how the reduction in cellular energy production and the consequent loss of consciousness and Will to Live allows human predators and parasites to run riot over the globe. The runaway psychopathic control grid uses malevolent Nazi techniques to dehumanize society into the slave machine population. Once the ever-widening control grid has been set up over multiple generations via social-control techniques (a lot of which were developed by the Nazis in WWII) then we have to find ways to exit or transcend the cultural mind in order to save our soul, our bloodline and anything of true value in human life.
We see clearly how the net of species decline is set when we look at how hypothyroidism and low thyroid (thyroxin) levels ties into lower cellular respiration and the flip over to glycolysis associated with cancer, heart disease, diabetes, neuropathy and aging. The lower activity of the pyruvate carrier in mitochondria from aging and hypothyroidism may be ascribed to changes in the lipid domain surrounding the carrier molecule in the mitochondrial membrane. And how by reinstating our “normal” mitochondrial levels of Cardiolipin fatty acid we can increase our oxy phos ATP production, and in so doing increase cell voltage and thus reestablish the high energy levels needed for health and sovereignty. Plus raising the DHA levels of Cardiolipin also reinstates the healthy cell death (apoptosis) necessary to avoid cancerous growth. With inferior cardiolipin both the life and death processes of the cell are undermined.
We can observe how loss of thyroid function leads to the loss of pyruvate conversion into ATP by studying what happens with excessive thyroid activity. When rats are made hyperthyroid, hormone-mediated changes in the cardiolipin composition of the mitochondrial membranes occurs; in particular, the negatively charged phospholipids such as cardiolipin and phosphatidylserine were found to increase by more than 50%. Plus minor alterations were found in the pattern of fatty acids with an increase in the ratio 20:4 to 18:2 molar. These changes in the mitochondrial phospholipid composition alter the kinetic parameters of pyruvate transport in mitochondria. This in turn amplifies the activity of the pyruvate carrier and stimulates pyruvate-dependent oxygen uptake by 35-40% in mitochondria, essentially greatly raising cell metabolism. (Yet to be substantiated: if pyruvate cannot freely enter into the mitochondria due to inferior mitochondrial membranes, this must mean that glucose levels would build up in the cytosol…stimulating the enzymes for glycolysis…thus transferring the fuel for oxy phos ATP production over the anaerobic fermentation method that produces only 2 ATP, compared to the larger amount of 36-38 ATP by oxy phos, wasting 95% of the potential glucose energy.)
Studies indicate that rat cardiac mitochondrial oxygen consumption and the enzymatic activity of cytochrome oxidase decreased as the quantity of cardiolipin (L4CL) was reduced when the fatty acid composition of the diet was changed. A loss of CL content and alterations in its composition, along with CL peroxidation have been associated with mitochondrial dysfunction in a variety of pathological conditions, including ischemia, hypothyroidism, diabetes, aging, and heart disease. It is clear therefore that changes in the quantity, content and structure of CL occur in mitochondrial dysfunction forming the basis of metabolic dysfunction and degenerative disease.
Heart mitochondria from hypothyroid rats translocate pyruvate much more slowly and have a parallel decrease of the rate of pyruvate-dependent oxygen uptake from normal rats. IN FROM HYPOTHYROID RATS THE HEART MITOCHONDRIAL FATTY ACID PATTERN IN THE MITOCHONDRIAL MEMBRANES WAS ALTERED, SUGGESTING THAT CHANGES IN THE LIPID ENVIRONMENT WHICH SURROUNDS THE PYRUVATE CARRIER MOLECULE IN THE MITOCHONDRIAL MEMBRANE RESULTS IN THE DECREASED ACTIVITY OF THE PYRUVATE TRANSLOCATOR.
Mitochondrial dysfunction can occur when the amount of CL declines due to enhanced CL degradation (e.g., hydrolysis by endogenous phospholipases) or by the reduced synthesis of new CL, as a result of impaired enzyme function or the unavailability of CL precursors. Aging also reduces the rate of pyruvate transport in mitochondria (38%) and is associated with the parallel lowering in the rate of pyruvate-dependent oxygen uptake. This loss of efficiency can be attributed to the fact that heart aging significantly alters the mitochondrial lipid composition. These changes include total cholesterol increases (43%), the phospholipids decrease (15%) and the cholesterol/phospholipid molar ratio increases (68%). Among phospholipids, it is cardiolipin that shows the greatest alteration (28% decrease in aged rats), perhaps because of its extra vulnerability to oxidation.
Cardiolipin may be particularly susceptible to free radical peroxidation because of the abundance of double bonds in its structure and its close association with respiratory chain proteins, which are known to be a major source of reactive oxygen species (ROS) in the mitochondria. Oxidative injury of mitochondria is widely believed to play an important role in the mitochondrial decay and dysfunction seen in aging and may contribute to an age-associated decline in CL. Loss of CL and composition alterations due to aging was closely associated with decreased activity of the mitochondrial phosphate transporter, pyruvate carrier, adenine nucleotide transporter, cytochrome oxidase, and the Acetyl-l-carnitine transporter.
Acetyl-l-carnitine’s major function in the body is to help transport long-chain fatty acids so they can be used for eventual energy production. It also helps maintain levels of coenzyme A (acetyl-CoA), which is essential for a number of metabolic reactions. Acetyl-l-carnitine also has neuroprotective, cardioprotective, cytoprotective, antioxidant and anti-apoptotic activity. Vitamin C is required for the synthesis of the carnitine that is needed for this transport of fat into mitochondria, for conversion to energy. Lifelong intake of powerful antioxidants both supplemental and in the diet will help preserve cardiolipin levels and maintain energy generation as we age. *Remember, simply taking increased Omega-3 into a highly oxidizing, inflammatory, high blood sugar/glycating, fermenting, demineralized, hypothyroid/low-voltage body will only add high quality fuel to the process of putrification and decay.
Supplementation with L-carnitine and α-lipoic acid reduces CL losses and the age-related increase in free radicals (hydrogen peroxide) in heart mitochondria. Interestingly, acetyl-carnitine effects are limited to preservation of "normal" CL levels, and may involve improved mitochondrial fatty acid import and a preservation of cellular high-energy phosphate content needed for ATP. Not surprisingly treatment of aged rats with acetyl-L-carnitine reversed the age-associated decline in cardiolipin content. As the changes in cardiolipin content were correlated with changes in rates of pyruvate transport and oxidation, it is thought that acetyl-L-carnitine reverses the age-related decline in the mitochondrial pyruvate metabolism by restoring the normal cardiolipin content.
Acetyl L carnitine stimulates the electron transport as does caffeine and Coenzyme Q10. Kelp or iodine is necessary to keep up the thyroxin levels needed for Cardiolipin synthesis, for the thyroid hormone is a major regulator of mitochondrial biogenesis, respiratory function and lipid metabolism and has been shown to directly modulate CL content by influencing the activity of CL biosynthesis enzymes. Thyroxin induces new CL synthesis by increasing the activities of CL synthase and phosphatidylglycerol phosphate synthase, and promotes the remodeling of CL. Conversely, low thyroxin or hypothyroidism decreases the activities of CL synthase resulting in a significant loss of CL content and the functioning of CL-dependent protein, which in turn are restored by treatment with thyroid hormone. Thus the loss of CL and associated mitochondrial protein function in the aged, hypothyroid, and ischemic rat heart have been effectively restored by reconstituting mitochondria CL with thyroxin, acetyl-carnitine and antioxidant therapy to restore CL levels and CL-dependent protein functions.