MITOCHONDRIAL DYSFUNCTION: PHOTOSYNTHESIS AND ATP: A SLOW PERSISTENT KILL
August 23, 2022
We have been lied to. All of us. On a scale that even I find to be unimaginable. I do not believe that what I have discovered is an “accident,” or “honest mistake.”
We have been looking at the behemoth of SARS-CoV-2 in the dark, each of us sensing our own niche of pathology while we miss defining the monstrous beast in its entirety. And, that beast, is without question, the engineered Spike Protein.
WHAT IS A SYSTEMIC HERBICIDE?
First, of course, systemic herbicides are used to kill WEEDS. What, then, pray tell, is a WEED? Well, what follows is a good summation. I leave it to the reader to extrapolate other “definitions.”
Systemic herbicides, also known as translocated herbicide are combinations of chemicals that are applied to the vegetative parts of a weed and are absorbed to the phloem and xylem tissue where they act in destroying weeds.
Systemic herbicides are different from contact in that they follow a slow process of action.
Contact herbicides work immediately, but systemic herbicides offer a more lasting solution to weed control.
This is because systemic herbicides are absorbed by the root of crops during photosynthesis which leads to the total death of the plant.
So, how do they work?
Most systemic herbicides work by disrupting the biochemical balance in weeds.
Prevalent phenoxy herbicides like 2,4 – D that are both systemic and selective mimic natural occurring plant chemical called Indole Acetic Acid (IAA).
This causes an imbalance in IAA which in turn cause inhibited growth, elongation, twisting, and starvation, then eventual death of the weed.
Also, when absorbed by plants, systemic herbicides are capable of interrupting photosynthesis.
They also release of hydroxyl compound that is toxic to the weeds. This process deprives weeds of essential nutrients and leads to their gradual destruction.
Systemic herbicides that target the enzyme plants in weeds will disrupt the sequence of a complex chemical reaction.
Thus, toxic substances are released to the weed system which kills the plant.
Systemic Herbicide: A Reliable Alternative Solution for Weed Control
HOW DOES THIS RELATE TO HUMAN BEINGS?
Systemic herbicides work by interrupting the energy conversion of photosynthesis. Photosynthesis is how plants generate their energy.
They do this the same way we do. With MITOCHONDRIA.
The mitochondrion converts the carbohydrates formed by photosynthesis into CO2 and H2O, with the energy going into the formation of ATP.
Photosynthesis is food production using the energy from sunlight.
Chloroplasts are the organelles where photosynthesis occurs.
Mitochondria are the organelles that convert the energy in food into ATP to be used as chemical energy by the cell.
How does a mitochondria relate to photosynthesis?
HOW DOES THIS RELATE TO THE SPIKE PROTEIN?
The Spike Protein is a supreme disruptor/destroyer/reprogrammer of mitochondria.
SARS-COV2 spike protein manipulates mitochondrial mechanisms to evade the host immune response and may alter mitochondrial functions leading to enhanced ROS production, perturbed signaling, and blunted antiviral defenses of the host. We speculate that SAR-COV-2 induces mitochondrial dysfunction and activation of the mitochondrial-dependent intrinsic apoptotic pathway, resulting in microglial and neuronal apoptosis. We examined the effect of a recombinant SARS-COV2 spike protein and heat inactivated SARS-COV2 on cytokine production, ROS /NOS production, mitochondrial bioenergetics, and the possible mechanisms that may underlie SAR-COV2 induced mitochondrial dysfunction in human microglial cells. Our results showed that microglia treated with SARS-COV2 release an increased amount of pro-inflammatory cytokines suggesting that SARS-COV2 induces an increased inflammatory response and cytokine dysregulation. SARS-COV2 also induces an increased level of oxidative stress, HIF-1α production and inflammasome activation, contributing to both mitochondrial dysfunction and increased ROS production.
Mitochondrial Dynamics in SARS-COV2 Spike Protein Treated Human Microglia: Implications for Neuro-COVID
ACUTE COVID DEATH AND LONG COVID AS A STATE OF SLOW DEATH
While the mitochondria are being destroyed, many pathological events occur before the organism dies. They should, by now, sound all too familiar.
A significant number of COVID-19 patients develop neurological symptoms, attributed to viral encephalitis, resulting in neuroinflammation, neuronal damage, and neurocognitive impairment. The microglia, which are the resident macrophages in the central nervous system, are the major players in the brain’s immune response to SARS-CoV-2 infection. Furthermore, it has been shown that functional mitochondria are integral to initiation and maintenance of immune responses by microglia, while neurological damage in COVID patients is attributed to mitochondrial dysfunction. Mitochondria are the primary site of ATP production and also regulate basic metabolic functions and participate in homeostasis, cellular proliferation, and apoptosis as well as in the synthesis of amino acids, lipids, and nucleotides.
Mitochondrial Dysfunction: A Prelude to Neuropathogenesis of SARS-CoV-2
IMMUNE DYSFUNCTION AND CYTOKINE STORM
Once inside the cell, SARS-CoV-2 triggers a massive inflammatory response. Through the innate immunity functions triggered upon viral infection detailed above, cytokines such as TNF-α, INF-γ, and interleukin-10 arrive at infected cells and cause an increase in mitochondrial ROS production through gene expression upregulation and electron transport chain modulation (Saleh et al., 2020). Mitochondrial ROS then stimulates additional proinflammatory cytokine production (Li et al., 2013) as the virus continues to persist, eventually leading to a “cytokine storm” in which over-inflammation can cause fatal harm if adaptive immunity does not take over in time. The immune response also causes the mitochondria to divert some energy away from ATP production to contribute to ROS production, which can harm the mitochondria in overwhelming amounts, leading to membrane permeabilization and apoptosis (Saleh et al., 2020). If severely damaged mitochondria release their contents into the cytosolic space, they stimulate the production of more cytokines such as IL-1β and IL-6 which are hallmarks for COVID-19 (Saleh et al., 2020).
Another mechanism of mitochondrial disruption employed by SARS-CoV-2 involves ferritin as evidenced by the high levels of ferritin in those with severe outcomes (Aguirre and Culotta, 2012). A normally functioning mitochondrion uses this iron to make heme, create iron-sulfur clusters, and store as mitochondrial ferritin (Saleh et al., 2020), but an overload of iron can lead to oxidative stress and impair mitochondrial function by reducing oxygen consumption by the mitochondria (Tang et al., 2020). Additionally, the ferritin overload can disrupt glucose tolerance in these cells with mitochondrial oxidative stress (Tang et al., 2020), which has implications for diabetic patients.
Aging cells embody senescence in part from an increase in mitochondrial dysfunction (Wiley et al., 2016). Given the negative effects on mitochondrial health by SARS-CoV-2 discussed previously, an aged person is starting with already weakened mitochondria and facing a disease that affects mitochondria. This progression can only lead to worsened outcomes. Senescence also affects macrophages, which have protective effects on the lungs during a SARS-CoV-2 infection; without properly functioning macrophages, the body’s response to SARS-CoV-2 will be weaker (Liu et al., 2020). Older individuals were also found to have increased levels of mtDNA in the cytoplasm (Pinti et al., 2014), and due to mtDNA’s role in inducing innate immunity and increasing inflammation, this is likely another mechanism that contributes to the lethal levels of inflammation seen in older COVID-19 patients.
Impact of COVID-19 on Mitochondrial-Based Immunity in Aging and Age-Related Diseases
SUDDEN CARDIAC DEATH
A 25-year-old, emaciated man without medical treatment was found to have died suddenly at home by his mother. At autopsy, there were no injuries to his body, but significant circulatory insufficiency was observed. Electron microscopy revealed abnormal mitochondria in cells of the cardiac conduction system. The conduction system was filled with mitochondrial size abnormalities and mitochondrial cristae abnormalities.
A case of sudden cardiac death due to mitochondrial disease
Mitochondria are often regarded as the powerhouse of the cell by generating the ultimate energy transfer molecule, ATP, which is required for a multitude of cellular processes. However, the role of mitochondria goes beyond their capacity to create molecular fuel, to include the generation of reactive oxygen species, the regulation of calcium, and activation of cell death. Mitochondrial dysfunction is part of both normal and premature ageing, but can contribute to inflammation, cell senescence, and apoptosis. Cardiovascular disease, and in particular atherosclerosis, is characterized by DNA damage, inflammation, cell senescence, and apoptosis. Increasing evidence indicates that mitochondrial damage and dysfunction also occur in atherosclerosis and may contribute to the multiple pathological processes underlying the disease.
Mitochondria in vascular disease
Here, we investigate the role of oxidative stress and mitochondrial dysfunction in the proatherothrombotic status of APS patients induced by IgG-antiphospholipid antibodies and the beneficial effects of supplementing cells with coenzyme Q(10) (CoQ(10)). A significant increase in relevant prothrombotic and inflammatory parameters in 43 APS patients was found compared with 38 healthy donors. Increased peroxide production, nuclear abundance of Nrf2, antioxidant enzymatic activity, decreased intracellular glutathione, and altered mitochondrial membrane potential were found in monocytes and neutrophils from APS patients. Accelerated atherosclerosis in APS patients was found associated with their inflammatory or oxidative status.
Mitochondrial dysfunction in antiphospholipid syndrome: implications in the pathogenesis of the disease and effects of coenzyme Q(10) treatment
Increasing evidence suggests that abnormally hyperphosphorylated tau plays a vital role in the pathogenesis of Alzheimer's disease (AD). Mitochondrial dysfunction also has a recognized role in the pathophysiology of AD. In recent years, mitochondrial dysfunction has been strongly associated with tau pathology in AD.
The Association of Tau With Mitochondrial Dysfunction in Alzheimer's Disease
DE NOVO DIABETES
Mitochondrial diabetes is caused by poor functioning of insulin-producing cells in the pancreas and/or by the emergence of insulin resistance as part of a mitochondrial disorder.
And what of those who are most at risk to COVID?
Trisomy of chromosome 21 (TS21) is the most common autosomal aneuploidy compatible with postnatal survival with a prevalence of 1 in 700 newborns. Its phenotype is highly complex with constant features, such as mental retardation, dysmorphic traits and hypotonia, and variable features including heart defects, susceptibility to Alzheimer’s disease (AD), type 2 diabetes, obesity and immune disorders. Overexpression of genes on chromosome-21 (Hsa21) is responsible for the pathogenesis of Down syndrome (DS) phenotypic features either in a direct or in an indirect manner since many Hsa21 genes can affect the expression of other genes mapping to different chromosomes. Many of these genes are involved in mitochondrial function and energy conversion, and play a central role in the mitochondrial dysfunction and chronic oxidative stress, consistently observed in DS subjects.
Mitochondrial dysfunction in down syndrome: molecular mechanisms and therapeutic targets
Mitochondrial deficit, altered redox balance and chronic low-grade inflammation are evident in schizophrenia. It is hypothesized that oxidative/nitrosative stress responses due to mitochondrial dysfunctions might activate immuno-inflammatory pathways and subsequently lead to neuroprogressive changes in schizophrenia.
Mitochondrial dysfunction in schizophrenia: pathways, mechanisms and implications
Can this be treated, halted, reversed? I certainly hope so.
The first step would be to realize that HUMAN BEINGS ARE NOT WEEDS.
Stop treating us as them.
Again, thanks to all for the kinds words and support. I will keep fighing the good fight.