For those of you who follow my work, you know that everything is based on flow. Life is only as a flow-dependent phenomena, and it occurs by balancing the flows of opposing forces, and the opposing forces that are balanced or those that produce free radicals and those that negate the production of free radicals, because free radicals disrupt the harmony of the complexity of the flow of life. This turns out to have incredible important effects and consequences for everything. But today, we’ll address the coronavirus issue.
What are the balancing acts that are going on there?
Angiotensin is a protein that is involved in regulating blood pressure. In doing that, it tends to be a pro-inflammatory phenomena, which is involved with sugar burning. In contrast, it can be modified by an enzyme that cleaves that initial protein product and makes shorter ones. A 9 peptide and a 7 peptide product can ultimately be produced from angiotensin. Angiotensin 1, angiotensin 2 are both broken down by angiotensin converting enzyme, and it turns out that that peptide as well as the angiotensin converting enzyme (angiotensin 2) all very involved with lipid metabolism. So look at this scenario: there’s an existing drug composed of the seven peptides that we know turns on fat burning and inhibits all sorts of negative consequences associated with angiotensin. Angiotensin converting enzyme, ACE2, to is the landing pad for the coronavirus, COVID-19.
So while on one hand it is involved in creating the problem, on the other hand it’s involved with fat burning, which turns off the ability of the virus and viruses in general to replicate. Because when they replicate, they make too many free radicals and that will kill them. So that’s balanced by turning on fat, burning via AMP Kinase, and other modes of accomplishing. That’s metabolic switch.
So the bottom line is there’s already an existing drug out there that I believe will be tremendously beneficial. And that is the angiotensin 2 converting enzyme peptide 1 through 7. It’s been shown to have all sorts of biological effects that are completely consistent with what I’ve been describing for years.
Now the balance between carbohydrate metabolism and differentiated cell functions versus fat burning and resurrecting the ability to have the differentiated functions by turning on cellular recycling and repair.
So we completely control HIV with high doses of cannabis and metabolic manipulation. Likewise for Kaposi’s sarcoma. Those are two totally different types of viruses. Karposi’s, being a herpes virus, a DNA virus and HIV being a negative stranded RNA virus. So here we are now dealing with COVID-19, which is a positive stranded RNA virus.
So it doesn’t matter what you’re looking at because any kind of living system, which is what a virus is when it’s infected, a cell is dependent on flow. The flow is always dependent on balancing carbohydrate metabolism with lipid metabolism, which means balancing differentiated abilities, biochemistry with resurrecting, restructuring, rebuilding biochemistry that’s associated with fat burning. That’s also, by the way, when bone sort of posited and telomeres are extended.
The following slides show the connection between the RAS (Renin/ Angiotensin) system, metabolism and the Corona virus. All metabolism works on the absolute need to balance opposing forces in order to minimize excess free radical production. The lethality of respiratory infections, as well as irritant chemical inhalation, is the free radical dependent development of ARDS (adult respiratory distress syndrome). The coronavirus attaches to ACE2 proteins on the surface of cells, especially those of the lung and kidney. The ACE2 protein creates heptapeptide ANG1-7 that protects against the negative effects of angiotensin by turning on fat burning (autophagy) that recycles free radical-damaged cellular components. Ang1-7, made by ACE2 acting on full sized membrane bound ANG, should compete with the virus and prevent the first step of a viral infection (entry). ANG1-7 is a commercially available FDA approved pharmaceutical.
THE RENIN-ANGIOTENSIN SYSTEM (RAS)
THE RENIN-ANGIOTENSIN SYSTEM (RAS) is an important regulator of
arterial blood pressure (BP). Angiotensin II (ANG II) is the major effector
molecule of the RAS, which exerts its biological effects mainly via the type 1
ANG II receptor (AT1R). Therefore, ANG II acts as a potent vasoconstrictor,
regulates water intake and salt metabolism, and increases sympathetic
outflow and blood pressure (Paul M, Poyan Mehr A, Kreutz R. Physiology of
local renin-angiotensin systems. Physiol Rev 86: 747–803, 2006).
Wikipedia: Angiotensin is a peptide hormone that causes vasoconstriction
and an increase in blood pressure. It is part of the renin–angiotensin system,
which regulates blood pressure. Angiotensin also stimulates the release of
aldosterone from the adrenal cortex to promote sodium retention by the
kidneys . Angiotensin source
ANG 1–7 treatment also suppressed the production of reactive oxygen species via attenuation of NADPH oxidase activity and reduced inflammation in perirenal adipose tissue. Furthermore, ANG 1–7 treatment decreased lipid accumulation in db/db kidneys, accompanied by increased expressions of renal adipose triglyceride lipase (ATGL). Alterations in ATGL expression correlated with increased SIRT1 expression and deacetylation of FOXO1. The up-regulation of angiotensin-converting enzyme 2 levels in diabetic nephropathy was normalized by ANG 1–7. ANG 1–7 treatment exerts renoprotective effects on diabetic nephropathy, associated with reduction of oxidative stress, inflammation, fibrosis, and lipotoxicity. ANG 1–7 can represent a
promising therapy for diabetic nephropathy. Angiotensin 1-7 Am J Physiol Renal Physiol 306: F812–F821, 2014. First published February 19, 2014; doi:10.1152/ajprenal.00655.2013
Angiotensin-converting enzymes ACE1 and ACE2 – homologues with different key functions in the renin–angiotensin system. ACE cleaves angiotensin I to generate angiotensin II
ACE2 inactivates angiotensin II and is a negative regulator of the system. ACE2 has also recently been identified as a potential SARS virus receptor The renin–angiotensin system has an important role in maintaining blood pressure homeostasis, as well as fluid and salt balance . ACE2 is a homologue of ACE, and functions a negative regulator of the renin–angiotensin system . Although ACE2 is expressed in the lungs of humans and mice, nothing is known about its function in the lungs. However, mortality following SARS coronavirus infections approaches almost 10%
“Here we report that ACE2 and the angiotensin II type 2 receptor (AT2) protect mice from severe acute lung injury induced by acid aspiration or sepsis”.
ACE2 inhibits breast cancer angiogenesis via suppressing the VEGFa/VEGFR2/ERK pathway
Excessive Glutamate Stimulation Impairs ACE2 Activity Through ADAM17-Mediated Shedding in Cultured Cortical Neurons
Neurons. Cell Mol Neurobiol 38, 1235-1243 (2018).
α-Lipoic Acid Reduces Neurogenic Hypertension by Blunting Oxidative StressMediated Increase in ADAM17. We previously reported that type 2 angiotensin-converting enzyme (ACE2) compensatory activity is impaired by the disintegrin and metalloprotease 17 (ADAM17), and lack of ACE2 is associated with oxidative stress in neurogenic hypertension.
Taken together, these data suggest that LA might preserve ACE2 compensatory activity by breaking the feedforward cycle between ADAM17 and oxidative stress, resulting in a reduction of neurogenic hypertension.
de Queiroz, T. M., Xia, H., Filipeanu, C. M., Braga, V. A. & Lazartigues, E.Am J Physiol Heart Circ Physiol 309,H926-34 (2015).
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