• Due to excessive bot signups along with nefarious actors we are limiting forum registration. Keep checking back for the register link to appear. Please do not send emails or have someone post to the forum asking for a signup link. Until the current climate changes we do not see a change of this policy. To join the forum you must have a compelling reason. Letting us know what skills/knowledge you will bring to the community along with the intent of your stay here will help in getting you approved.

Minerals and vitamins that act like blood thinning agents-hack ,,covid injections"

ruprmurdoch

Member
Joined
Mar 22, 2017
Messages
77
I just understood that all deaths due to covid injections are mostly results of blood clot. They treat it by blood thinners. So if someone have to take ,,this", he/she should increase blood thinning vitamins and minerals ingestion. Vitamin E and garlic are blood thinners, on the other hand Vitamin K and coenzyme Q10 are increasing coagulation of blood. What is Your thought about what I wrote ?
 

haidut

Member
Joined
Mar 18, 2013
Messages
18,170
Location
USA / Europe
I just understood that all deaths due to covid injections are mostly results of blood clot. They treat it by blood thinners. So if someone have to take ,,this", he/she should increase blood thinning vitamins and minerals ingestion. Vitamin E and garlic are blood thinners, on the other hand Vitamin K and coenzyme Q10 are increasing coagulation of blood. What is Your thought about what I wrote ?
Aspirin, progesterone, vitamin D, anti-serotonin chemicals, etc are also blood thinners. The problem is that this addresses only the short-term side effects - i.e. the clotting. We don't know exactly what the long term side effects are and how to protect against them. Judging from the animal studies, there is a multitude of severe side effects, leading to most of the animals in the studies dying. Some of those side effects were various types of cancer, lethal neurological disease, immune failure (e.g. AIDS), etc and I would rather not get to such a state and then wonder how to treat it. Also, if the mRNA/DNA from the vaccines gets incorporated into your DNA then it is very bad news not only for you but also for your offspring (if you get to even keep your fertility, since vaccines affect that too) and all generations down the road descended from you. Does all that sound like something worth the risk of taking the vaccine? Especially considering the vaccine is not even effective for the very purpose(s) its pushers parrot about on mainstream media.
 

ruprmurdoch

Member
Thread starter
Joined
Mar 22, 2017
Messages
77
Aspirin, progesterone, vitamin D, anti-serotonin chemicals, etc are also blood thinners. The problem is that this addresses only the short-term side effects - i.e. the clotting. We don't know exactly what the long term side effects are and how to protect against them. Judging from the animal studies, there is a multitude of severe side effects, leading to most of the animals in the studies dying. Some of those side effects were various types of cancer, lethal neurological disease, immune failure (e.g. AIDS), etc and I would rather not get to such a state and then wonder how to treat it. Also, if the mRNA/DNA from the vaccines gets incorporated into your DNA then it is very bad news not only for you but also for your offspring (if you get to even keep your fertility, since vaccines affect that too) and all generations down the road descended from you. Does all that sound like something worth the risk of taking the vaccine? Especially considering the vaccine is not even effective for the very purpose(s) its pushers parrot about on mainstream media.
I support and agree all You said, but I also look for ,,damage limitation" way. If this mRNA/DNA stuff is incorporated in our DNA it should be also way to remove it, beacuse there is epigenetic, so I think that certain supplementation and behaviour can diminish way of how this dangerous substance is working on our body.
 

Sofia2020

Member
Joined
May 25, 2020
Messages
333
I was so wrong, when I thought that Ray Peat was a bit paranoid, he just understand things better then I do.
 

md_a

Member
Joined
Aug 31, 2015
Messages
399
One of the body's defenses against angiotensin and circulatory problems is ACE2. The `virus`, vaccine, antivirals expose the body to spike protein or different stressors that reduces ACE2 and blocks the body's anti-inflammatory and anti-coagulation response. Things that increase ACE2 and reduce AT1 should work.

I took three studies at random.

……….

A renin-angiotensin level that is inappropriately high for the systemic blood pressure and the state of sodium balance is now recognized to be one of the modifiable cardiovascular risk factors. Angiotensin acts both as a circulating hormone and as a locally acting paracrine/autocrine/intracrine factor. The adverse effects of angiotensin on the heart include the mechanical results of elevated resistance to the pumping function of the myocardium, as well as the effects of neurohumoral abnormalities on various cardiac structures. In addition, cardiac damage follows acute ischaemic injury or chronic energy starvation due to coronary artery disease, attributable to either mechanical obstruction (atherosclerotic and/or thrombotic) or functional stenosis (vasospasm). Activation of the renin-angiotensin system has several haemodynamic and humoral consequences, all of which may damage the myocardium. These include acute myocardial ischaemia, left-ventricular hypertrophy, arrhythmias, alterations in the coagulation–fibrinolysis equilibrium, increased oxi- dative stress, and pro-inflammatory activity.

Angiotensin II exerts several direct effects on the heart via activation of the angiotensin type-1 receptor (AT1 receptor)
, which is a G-protein-linked receptor identified on cardiac myocytes that activates protein kinase C through formation of diacylglycerol and hydrolysis of phosphatidylinositol.17,18 The positive inotropic, mitogenic and arrhythmo- genic actions of A II are now well documented.19,20 It stimulates both hypertrophy and hyperplasia of cardiac myocytes as well as vascular smooth-muscle cells by activating proto-oncogenes, which is one of the early steps in cell hypertrophy and division. Intracellular second messengers generated by stimulation of AT1 receptors, such as phospholipases and phosphatidic acid, are now known to enhance mitogenesis; they were shown to increase thymidine incorporation in various cells,21,22 and induce mRNA expression of c-fos and c-myc.23 In fact, a close correlation has been reported in experimental animals between LVH and myocardial levels of A II.24 In addition to its direct action of stimulating protein synthesis and cell proliferation, A II has also been shown to release other growth factors from smooth-muscle cells and blood cells, such as the platelet-derived growth factor. Furthermore, it enhances peripheral sympathetic activity and exerts a permissive action on the release of noradrenaline,25 which possesses trophic properties of its own and promotes myocardial cell growth and hypertrophy.26

In addition to vasoconstriction-induced myocardial ischaemia, A II promotes myocardial damage by affecting normal oxygen metabolism. This exerts both direct deleterious effects on myocardial (and other) cells, and indirect effects via enhanced lipid peroxidation and atherogenesis leading to coronary artery disease.


Angiotensin II causes increased activity of the NADH and NADPH oxidases, with production of large amounts of superoxide anions.30 The data suggest that reactive oxygen intermediates may be part of the normal intracellular signalling responses following stimulation of AT1 receptors. Reactive oxygen species are known to cause oxidative damage to various cellular structures, including membranes, proteins such as intracellular enzymes, DNA sequences and DNA repair enzymes.31 Acute myocardial infarction is accompanied by activation of numerous systemic and local neurohumoral factors, including the renin-angiotensin system.32,33 Furthermore, reperfusion of the acutely infarcted area (as obtained experimentally by removal of a coronary ligature and clinically by thrombolytic agents) produces a surge in reactive oxygen species, causing tissue damage beyond that inflicted by ischaemia34 and partially attributed to activation of local humoral factors, including A II.

Another type of oxidative damage that is relevant to coronary heart disease is lipid peroxidation, which is the auto-oxidation of polyunsaturated fatty acid chains of lipids.37 Recent evidence indicates that low-density lipoprotein (LDL) cholesterol has to be oxidized before it becomes atherogenic, and that lipid peroxidation is the first step in this process. Oxidized LDL is taken up by macrophages, stimulates monocyte adhesion to the endothelium, inhibits vasodilation and is generally cytotoxic.38 Recent clinical work suggests that LDL cholesterol derived from hypertensive patients has an increased susceptibility to lipid peroxidation, which the authors attributed to A II


This mechanism would partly explain the increased tendency of hypertensive patients to develop atherosclerotic changes, leading to coronary obstruction as well as peripheral vascular obstructive disease. In fact, there is epidemiological evidence to suggest that high-renin-hypertensive patients are significantly more prone to heart attacks40,41 and to coronary disease in general.

Normal blood rheology depends on the constant equilibrium between forces that enhance intravascular coagulation and intrinsic thrombolytic factors. Disturbance of this process, by inhibitors of the tissue-type plasminogen activator (t-PA), for example, will tilt the balance towards increased thrombogenesis.47 In fact, elevated levels of the PA inhibitor-1 (PAI-1) have been implicated in the pathogenesis of thromboembolic diseases in general,48 and are considered to be a risk factor and/or marker for recurrence of myocardial infarction.49 Angiotensin II was reported to induce secretion of PAI-1 from cultured cells in vitro.50

In vivo infusions of A II in both hypertensive patients and normotensive control subjects were found to induce a rapid dose-dependent increase in circulating levels of PAI-1.51 The finding that A II enhances endothelial synthesis and secretion of PAI-1 suggests an additional mechanism by which activation of the renin-angiotensin system may increase the risk of coronary events. These data are consistent with the epidemiological studies linking high-renin hypertension to increased risk of heart attack, as mentioned earlier.40,41

Angiotensin II as a cardiovascular risk factor - Journal of Human Hypertension

…………….

Summary

There is an increased number of in vitro evidence that angioten-sin II (Ang II) may promote thrombosis. However there are no in vivo experiments exploring the effect of Ang II on thrombus formation. In the present study we have investigated the influence of Ang II on venous thrombosis in renovascular hypertensive rats. Furthermore, we examined the role of AT1 receptor and Ang II metabolites: angiotensin III (Ang III) and angioten-sin IV (Ang IV) in the mechanisms of Ang II action. The contribution of coagulation and fibrinolytic systems in the mode of Ang II action was also determined. Venous thrombosis was induced by ligation of vena cava. Ang II infused into rats developing venous thrombosis caused dose-dependent increase in thrombus weight, which was partially reversed by losartan, selective AT1 antagonist. Ang III did not influence the thrombus formation in hypertensive rats, while Ang IV caused a marked increase in thrombus weight only in one of the used doses. Our study shows that Ang II via AT1 receptor enhances thrombosis development. The prothrombotic effect of Ang II may partially depend on enhanced leukocytes adhesion to endothelial cells accompanied by accelerated fibrin formation and increased plasma level of PAI-1. Moreover, Ang II action is partially mediated by one of its metabolites – Ang IV.

Thieme E-Journals - Thrombosis and Haemostasis / Abstract

………..

The monocarboxypeptidase, ACE2, which is predominantly expressed in the heart and kidneys shuttles angiotensin metabolism away from the formation of Ang II thereby functioning essentially as a negative regulator of the RAS [2]. In human heart failure, there is upregulation of ACE2 which may provide a key adaptive and cardioprotective mechanism [7–9]. Our current study shows that in the absence of ACE2, cumulative damage from Ang II acting via the AT1 receptors is the predominant cause of the age-dependent cardiomyopathy. The phenotypic alterations in our mouse models closely mimic the biochemical, structural and functional alterations in human heart failure. The AT1 receptor blocker, irbesartan, slowed the progression to heart failure in Ace2−/y mutant mice which is consistent with the use of AT1 receptor blockers as effective therapy for human heart failure. Consistent with the increased oxidative stress in the myocardium, loss of ACE2 also leads to Ang II-dependent renal oxidative damage and glomerular injury [6] which together with possible vascular injury may in part contribute to the overall age-dependent cardiomyopathy in ACE2 null mice.

We have shown that in aged Ace2−/y mice, increased Ang II action via AT1 receptors was associated with enhanced pathological hypertrophy, ventricular dilation and compromised systolic function. Ang II can induce reactive oxygen species such as H2O2 (hydrogen peroxide) and O2− (superoxide) formation via activation of NADPH oxidase [3,20,21,40,41]. Ang II-mediated activation of the NADPH oxidase complex via AT1 receptors has been well documented in cardiomyocytes, vascular and endothelial cells [17,21,40]. Reactive oxygen species interact with nitric oxide which may deplete endogenous nitric oxide [42] while also leading to the formation of reactive and toxic species such as peroxynitrite (ONOO−) [3,21,40]. NADPH oxidase activity is increased in human heart failure which may facilitate the negative inotropic effects of Ang II [41,43]. We observed a marked increase in Ang II-dependent infiltration of neutrophils into the myocardium in ACE2-deficient hearts which was markedly reduced by AT1 receptor blockade. Ang II mediates a wide variety of cardiac inflammatory processes and leads to an upregulation of proinflammatory markers [22,23,44]. Ang II-mediated recruitment and activation of neutrophils perpetuate the free radical induced myocardial injury [20,45] and increase collagenase activity via the induction of MMP-8 expression which can degrade the extracellular matrix thereby compromising systolic function [18]. The activation of MAPK pathways is a characteristic finding in heart disease and plays a key role in the progression to heart failure [24]. Our data confirms the activation of myocardial MAPK pathways in aged Ace2−/y mutant mice and is consistent with changes observed following pressure-overload in young Ace2−/y mutant mice [19]. Indeed, ERK1/2, JNK1/2 and p38 pathways were all activated in Ace2−/y mutant mice and while AT1 blockade maintained the phosphorylation of the adaptive ERK1/2, activation of the maladaptive, JNK1/2 and p38, was selectively reduced.

Angiotensin II-mediated oxidative stress and inflammation mediate the age-dependent cardiomyopathy in ACE2 null mice
 

StephanF

Member
Joined
Jul 8, 2014
Messages
462
Location
Reno
Zeta Aid, it contains electrolytes that increase colloidal stability by strengthening the Zeta Potential of the blood. The blood particles become electrically charged up and repell each other. Zeta Aid contains potassium citrate and other electrolytes.



I posted on this subject several times.
 

Mauritio

Member
Joined
Feb 26, 2018
Messages
3,283
One of the body's defenses against angiotensin and circulatory problems is ACE2. The `virus`, vaccine, antivirals expose the body to spike protein or different stressors that reduces ACE2 and blocks the body's anti-inflammatory and anti-coagulation response. Things that increase ACE2 and reduce AT1 should work.

I took three studies at random.

……….

A renin-angiotensin level that is inappropriately high for the systemic blood pressure and the state of sodium balance is now recognized to be one of the modifiable cardiovascular risk factors. Angiotensin acts both as a circulating hormone and as a locally acting paracrine/autocrine/intracrine factor. The adverse effects of angiotensin on the heart include the mechanical results of elevated resistance to the pumping function of the myocardium, as well as the effects of neurohumoral abnormalities on various cardiac structures. In addition, cardiac damage follows acute ischaemic injury or chronic energy starvation due to coronary artery disease, attributable to either mechanical obstruction (atherosclerotic and/or thrombotic) or functional stenosis (vasospasm). Activation of the renin-angiotensin system has several haemodynamic and humoral consequences, all of which may damage the myocardium. These include acute myocardial ischaemia, left-ventricular hypertrophy, arrhythmias, alterations in the coagulation–fibrinolysis equilibrium, increased oxi- dative stress, and pro-inflammatory activity.

Angiotensin II exerts several direct effects on the heart via activation of the angiotensin type-1 receptor (AT1 receptor)
, which is a G-protein-linked receptor identified on cardiac myocytes that activates protein kinase C through formation of diacylglycerol and hydrolysis of phosphatidylinositol.17,18 The positive inotropic, mitogenic and arrhythmo- genic actions of A II are now well documented.19,20 It stimulates both hypertrophy and hyperplasia of cardiac myocytes as well as vascular smooth-muscle cells by activating proto-oncogenes, which is one of the early steps in cell hypertrophy and division. Intracellular second messengers generated by stimulation of AT1 receptors, such as phospholipases and phosphatidic acid, are now known to enhance mitogenesis; they were shown to increase thymidine incorporation in various cells,21,22 and induce mRNA expression of c-fos and c-myc.23 In fact, a close correlation has been reported in experimental animals between LVH and myocardial levels of A II.24 In addition to its direct action of stimulating protein synthesis and cell proliferation, A II has also been shown to release other growth factors from smooth-muscle cells and blood cells, such as the platelet-derived growth factor. Furthermore, it enhances peripheral sympathetic activity and exerts a permissive action on the release of noradrenaline,25 which possesses trophic properties of its own and promotes myocardial cell growth and hypertrophy.26

In addition to vasoconstriction-induced myocardial ischaemia, A II promotes myocardial damage by affecting normal oxygen metabolism. This exerts both direct deleterious effects on myocardial (and other) cells, and indirect effects via enhanced lipid peroxidation and atherogenesis leading to coronary artery disease.


Angiotensin II causes increased activity of the NADH and NADPH oxidases, with production of large amounts of superoxide anions.30 The data suggest that reactive oxygen intermediates may be part of the normal intracellular signalling responses following stimulation of AT1 receptors. Reactive oxygen species are known to cause oxidative damage to various cellular structures, including membranes, proteins such as intracellular enzymes, DNA sequences and DNA repair enzymes.31 Acute myocardial infarction is accompanied by activation of numerous systemic and local neurohumoral factors, including the renin-angiotensin system.32,33 Furthermore, reperfusion of the acutely infarcted area (as obtained experimentally by removal of a coronary ligature and clinically by thrombolytic agents) produces a surge in reactive oxygen species, causing tissue damage beyond that inflicted by ischaemia34 and partially attributed to activation of local humoral factors, including A II.

Another type of oxidative damage that is relevant to coronary heart disease is lipid peroxidation, which is the auto-oxidation of polyunsaturated fatty acid chains of lipids.37 Recent evidence indicates that low-density lipoprotein (LDL) cholesterol has to be oxidized before it becomes atherogenic, and that lipid peroxidation is the first step in this process. Oxidized LDL is taken up by macrophages, stimulates monocyte adhesion to the endothelium, inhibits vasodilation and is generally cytotoxic.38 Recent clinical work suggests that LDL cholesterol derived from hypertensive patients has an increased susceptibility to lipid peroxidation, which the authors attributed to A II


This mechanism would partly explain the increased tendency of hypertensive patients to develop atherosclerotic changes, leading to coronary obstruction as well as peripheral vascular obstructive disease. In fact, there is epidemiological evidence to suggest that high-renin-hypertensive patients are significantly more prone to heart attacks40,41 and to coronary disease in general.

Normal blood rheology depends on the constant equilibrium between forces that enhance intravascular coagulation and intrinsic thrombolytic factors. Disturbance of this process, by inhibitors of the tissue-type plasminogen activator (t-PA), for example, will tilt the balance towards increased thrombogenesis.47 In fact, elevated levels of the PA inhibitor-1 (PAI-1) have been implicated in the pathogenesis of thromboembolic diseases in general,48 and are considered to be a risk factor and/or marker for recurrence of myocardial infarction.49 Angiotensin II was reported to induce secretion of PAI-1 from cultured cells in vitro.50

In vivo infusions of A II in both hypertensive patients and normotensive control subjects were found to induce a rapid dose-dependent increase in circulating levels of PAI-1.51 The finding that A II enhances endothelial synthesis and secretion of PAI-1 suggests an additional mechanism by which activation of the renin-angiotensin system may increase the risk of coronary events. These data are consistent with the epidemiological studies linking high-renin hypertension to increased risk of heart attack, as mentioned earlier.40,41

Angiotensin II as a cardiovascular risk factor - Journal of Human Hypertension

…………….

Summary

There is an increased number of in vitro evidence that angioten-sin II (Ang II) may promote thrombosis. However there are no in vivo experiments exploring the effect of Ang II on thrombus formation. In the present study we have investigated the influence of Ang II on venous thrombosis in renovascular hypertensive rats. Furthermore, we examined the role of AT1 receptor and Ang II metabolites: angiotensin III (Ang III) and angioten-sin IV (Ang IV) in the mechanisms of Ang II action. The contribution of coagulation and fibrinolytic systems in the mode of Ang II action was also determined. Venous thrombosis was induced by ligation of vena cava. Ang II infused into rats developing venous thrombosis caused dose-dependent increase in thrombus weight, which was partially reversed by losartan, selective AT1 antagonist. Ang III did not influence the thrombus formation in hypertensive rats, while Ang IV caused a marked increase in thrombus weight only in one of the used doses. Our study shows that Ang II via AT1 receptor enhances thrombosis development. The prothrombotic effect of Ang II may partially depend on enhanced leukocytes adhesion to endothelial cells accompanied by accelerated fibrin formation and increased plasma level of PAI-1. Moreover, Ang II action is partially mediated by one of its metabolites – Ang IV.

Thieme E-Journals - Thrombosis and Haemostasis / Abstract

………..

The monocarboxypeptidase, ACE2, which is predominantly expressed in the heart and kidneys shuttles angiotensin metabolism away from the formation of Ang II thereby functioning essentially as a negative regulator of the RAS [2]. In human heart failure, there is upregulation of ACE2 which may provide a key adaptive and cardioprotective mechanism [7–9]. Our current study shows that in the absence of ACE2, cumulative damage from Ang II acting via the AT1 receptors is the predominant cause of the age-dependent cardiomyopathy. The phenotypic alterations in our mouse models closely mimic the biochemical, structural and functional alterations in human heart failure. The AT1 receptor blocker, irbesartan, slowed the progression to heart failure in Ace2−/y mutant mice which is consistent with the use of AT1 receptor blockers as effective therapy for human heart failure. Consistent with the increased oxidative stress in the myocardium, loss of ACE2 also leads to Ang II-dependent renal oxidative damage and glomerular injury [6] which together with possible vascular injury may in part contribute to the overall age-dependent cardiomyopathy in ACE2 null mice.

We have shown that in aged Ace2−/y mice, increased Ang II action via AT1 receptors was associated with enhanced pathological hypertrophy, ventricular dilation and compromised systolic function. Ang II can induce reactive oxygen species such as H2O2 (hydrogen peroxide) and O2− (superoxide) formation via activation of NADPH oxidase [3,20,21,40,41]. Ang II-mediated activation of the NADPH oxidase complex via AT1 receptors has been well documented in cardiomyocytes, vascular and endothelial cells [17,21,40]. Reactive oxygen species interact with nitric oxide which may deplete endogenous nitric oxide [42] while also leading to the formation of reactive and toxic species such as peroxynitrite (ONOO−) [3,21,40]. NADPH oxidase activity is increased in human heart failure which may facilitate the negative inotropic effects of Ang II [41,43]. We observed a marked increase in Ang II-dependent infiltration of neutrophils into the myocardium in ACE2-deficient hearts which was markedly reduced by AT1 receptor blockade. Ang II mediates a wide variety of cardiac inflammatory processes and leads to an upregulation of proinflammatory markers [22,23,44]. Ang II-mediated recruitment and activation of neutrophils perpetuate the free radical induced myocardial injury [20,45] and increase collagenase activity via the induction of MMP-8 expression which can degrade the extracellular matrix thereby compromising systolic function [18]. The activation of MAPK pathways is a characteristic finding in heart disease and plays a key role in the progression to heart failure [24]. Our data confirms the activation of myocardial MAPK pathways in aged Ace2−/y mutant mice and is consistent with changes observed following pressure-overload in young Ace2−/y mutant mice [19]. Indeed, ERK1/2, JNK1/2 and p38 pathways were all activated in Ace2−/y mutant mice and while AT1 blockade maintained the phosphorylation of the adaptive ERK1/2, activation of the maladaptive, JNK1/2 and p38, was selectively reduced.

Angiotensin II-mediated oxidative stress and inflammation mediate the age-dependent cardiomyopathy in ACE2 null mice
It should help ,but it might not be enough. I just posted a study about the spike protein increasing inflammation via a ACE2-independent mechanism, namely Tlr4 agonism.
 

Lollipop2

Member
Joined
Nov 18, 2019
Messages
3,161
I was so wrong, when I thought that Ray Peat was a bit paranoid, he just understand things better then I do.
That is the thing about Ray, his clarity never ceases to amaze me. Now research is surfacing that shows many of his understandings are accurate. Many people have tried to show that Ray is wrong over many issues throughout the years and he keeps outlasting everyone of them.
 

md_a

Member
Joined
Aug 31, 2015
Messages
399
It should help ,but it might not be enough. I just posted a study about the spike protein increasing inflammation via a ACE2-independent mechanism, namely Tlr4 agonism.
yes, thanks!

TLR4 is expressed on the surface of different cell types including endothelial cells and VSMCs, and is involved in the recognition of and response to LPS, although many non-infectious endogenous TLR4 ligands also exist [4], [20], [21]. There is evidence regarding a role for the TLR4 signaling pathway and the innate immune response in the development of cardiovascular pathologies with an inflammatory component such as atherosclerosis [14], diabetes [26][28] and pre-eclampsia [29], [30]. Hypertension has also been considered as a low-grade inflammatory disease, and growing evidence shows that the immune system is involved in the pathophysiology of hypertension [2][4].

RAS contributes to the vascular alterations associated with hypertension via its proinflammatory activity in the vascular wall, including the production of ROS, cytokines and prostanoids [1], [6], [36]. Furthermore, Ang II is able to induce the inflammatory response via the TLR4 pathway [13][19]; in addition, AT1 receptor blockers (ARBs) reduce the LPS-induced innnate immune response [41][43] and protect against myocardial ischemia-reperfusion injury through the TLR4/NF-κB signaling pathway [44]. Accordingly, we found that Ang II increased TLR4 mRNA levels in SHR VSMCs via the AT1 receptors, and treatment of SHRs with losartan in vivo decreased the increased TLR4 levels found in this strain. These results suggest that the increased RAS activity observed in hypertension contributes to the increased TLR4 levels.

Hypertension is associated with functional vascular alterations such as endothelial dysfunction with impaired endothelium-dependent relaxations and increased vasoconstrictor responses. Endothelial dysfunction is a prognostic factor for cardiovascular events in patients with essential hypertension [45]. Our results demonstrate that the anti-TLR4 antibody treatment improved the vasodilator responses to acetylcholine in SHRs. Additionally, the anti-TLR4 antibody reduced vasoconstrictor responses to phenylephrine, in agreement with results obtained in mesenteric resistance arteries [32]. Moreover, the increased phenylephrine response after endothelial denudation was greater in anti-TLR4 antibody-treated SHRs. Altogether, this study suggests for the first time, to the best of our knowledge, that TLR4 contributes to the endothelial dysfunction observed in hypertension. In keeping with this, our group and others have previously shown that LPS administration induces endothelial dysfunction in both peripheral [46], [47] and cerebral arteries [9]. Additionally, Liang et al. [48] reported that the in vivo and in vitro administration of LPS causes endothelial dysfunction in the arteries of wild-type mice, but not those of TLR4-mutated mice. The proposed role of TLR4 in endothelial dysfunction and the above mentioned increased TLR4 expression found in hypertensive animals can explain the greater impairment of bradykinin-induced relaxation elicited by LPS that was observed in the middle cerebral arteries of hypertensive rats [9].

Toll-Like Receptor 4 Upregulation by Angiotensin II Contributes to Hypertension and Vascular Dysfunction through Reactive Oxygen Species Production

...........

Cross talk between AT1 receptors and Toll-like receptor 4 in microglia contributes to angiotensin II-derived ROS production in the hypothalamic paraventricular nucleus​

ANG II is thought to increase sympathetic outflow by increasing oxidative stress and promoting local inflammation in the paraventricular nucleus (PVN) of the hypothalamus. However, the relative contributions of inflammation and oxidative stress to sympathetic drive remain poorly understood, and the underlying cellular and molecular targets have yet to be examined. ANG II has been shown to enhance Toll-like receptor (TLR)4-mediated signaling on microglia. Thus, in the present study, we aimed to determine whether ANG II-mediated activation of microglial TLR4 signaling is a key molecular target initiating local oxidative stress in the PVN. We found TLR4 and ANG II type 1 (AT1) receptor mRNA expression in hypothalamic microglia, providing molecular evidence for the potential interaction between these two receptors. In hypothalamic slices, ANG II induced microglial activation within the PVN (∼65% increase, P < 0.001), an effect that was blunted in the absence of functional TLR4. ANG II increased ROS production, as indicated by dihydroethidium fluorescence, within the PVN of rats and mice (P < 0.0001 in both cases), effects that were also dependent on the presence of functional TLR4. The microglial inhibitor minocycline attenuated ANG II-mediated ROS production, yet ANG II effects persisted in PVN single-minded 1-AT1a knockout mice, supporting the contribution of a non-neuronal source (likely microglia) to ANG II-driven ROS production in the PVN. Taken together, these results support functional interactions between AT1 receptors and TLR4 in mediating ANG II-dependent microglial activation and oxidative stress within the PVN. More broadly, our results support a functional interaction between the central renin-angiotensin system and innate immunity in the regulation of neurohumoral outflows from the PVN.


........

Hypertension is a multifactorial disease. Although a number of different underlying mechanisms have been learned from the various experimental models of the disease, hypertension still poses challenges for treatment. Angiotensin II plays an unquestionable role in blood pressure regulation acting through central and peripheral mechanisms. During hypertension, dysregulation of the Renin-Angiotensin System is associated with increased expression of pro-inflammatory cytokines and reactive oxygen species causing kidney damage, endothelial dysfunction, and increase in sympathetic activity, among other damages, eventually leading to decline in organ function. Recent studies have shown that these effects involve both the innate and the adaptive immune response. The contribution of adaptive immune responses involving different lymphocyte populations in various models of hypertension has been extensively studied. However, the involvement of the innate immunity mediating inflammation in hypertension is still not well understood. The innate and adaptive immune systems intimately interact with one another and are essential to an effectively functioning of the immune response; hence, the importance of a better understanding of the underlying mechanisms mediating innate immune system during hypertension. In this review, we aim to discuss mechanisms linking Angiotensin II and the innate immune system, in the pathogenesis of hypertension. The newest research investigating Angiotensin II triggering toll like receptor 4 activation in the kidney, vasculature and central nervous system contributing to hypertension will be discussed. Understanding the role of the innate immune system in the development of hypertension may bring to light new insights necessary to improve hypertension management.


1-s2.0-S1043661816309100-fx1_lrg.jpg
 

tankasnowgod

Member
Joined
Jan 25, 2014
Messages
6,750
Same . A year ago I thought vaccine passports was a conspiracy .
A year ago, it was. Remember, the definition of "conspiracy" is "a secret plan made by two or more people to do something that is harmful or illegal."

Although, seeing as some people (like Gates) were announcing this sort of thing, it may not have been "secret" by that point.
 

Badger

Member
Joined
Jan 23, 2017
Messages
662
Zeta Aid, it contains electrolytes that increase colloidal stability by strengthening the Zeta Potential of the blood. The blood particles become electrically charged up and repell each other. Zeta Aid contains potassium citrate and other electrolytes.



I posted on this subject several times.

In your view, would Zeta Aid cure Afib?
 

Mauritio

Member
Joined
Feb 26, 2018
Messages
3,283
yes, thanks!

TLR4 is expressed on the surface of different cell types including endothelial cells and VSMCs, and is involved in the recognition of and response to LPS, although many non-infectious endogenous TLR4 ligands also exist [4], [20], [21]. There is evidence regarding a role for the TLR4 signaling pathway and the innate immune response in the development of cardiovascular pathologies with an inflammatory component such as atherosclerosis [14], diabetes [26][28] and pre-eclampsia [29], [30]. Hypertension has also been considered as a low-grade inflammatory disease, and growing evidence shows that the immune system is involved in the pathophysiology of hypertension [2][4].

RAS contributes to the vascular alterations associated with hypertension via its proinflammatory activity in the vascular wall, including the production of ROS, cytokines and prostanoids [1], [6], [36]. Furthermore, Ang II is able to induce the inflammatory response via the TLR4 pathway [13][19]; in addition, AT1 receptor blockers (ARBs) reduce the LPS-induced innnate immune response [41][43] and protect against myocardial ischemia-reperfusion injury through the TLR4/NF-κB signaling pathway [44]. Accordingly, we found that Ang II increased TLR4 mRNA levels in SHR VSMCs via the AT1 receptors, and treatment of SHRs with losartan in vivo decreased the increased TLR4 levels found in this strain. These results suggest that the increased RAS activity observed in hypertension contributes to the increased TLR4 levels.

Hypertension is associated with functional vascular alterations such as endothelial dysfunction with impaired endothelium-dependent relaxations and increased vasoconstrictor responses. Endothelial dysfunction is a prognostic factor for cardiovascular events in patients with essential hypertension [45]. Our results demonstrate that the anti-TLR4 antibody treatment improved the vasodilator responses to acetylcholine in SHRs. Additionally, the anti-TLR4 antibody reduced vasoconstrictor responses to phenylephrine, in agreement with results obtained in mesenteric resistance arteries [32]. Moreover, the increased phenylephrine response after endothelial denudation was greater in anti-TLR4 antibody-treated SHRs. Altogether, this study suggests for the first time, to the best of our knowledge, that TLR4 contributes to the endothelial dysfunction observed in hypertension. In keeping with this, our group and others have previously shown that LPS administration induces endothelial dysfunction in both peripheral [46], [47] and cerebral arteries [9]. Additionally, Liang et al. [48] reported that the in vivo and in vitro administration of LPS causes endothelial dysfunction in the arteries of wild-type mice, but not those of TLR4-mutated mice. The proposed role of TLR4 in endothelial dysfunction and the above mentioned increased TLR4 expression found in hypertensive animals can explain the greater impairment of bradykinin-induced relaxation elicited by LPS that was observed in the middle cerebral arteries of hypertensive rats [9].

Toll-Like Receptor 4 Upregulation by Angiotensin II Contributes to Hypertension and Vascular Dysfunction through Reactive Oxygen Species Production

...........

Cross talk between AT1 receptors and Toll-like receptor 4 in microglia contributes to angiotensin II-derived ROS production in the hypothalamic paraventricular nucleus​

ANG II is thought to increase sympathetic outflow by increasing oxidative stress and promoting local inflammation in the paraventricular nucleus (PVN) of the hypothalamus. However, the relative contributions of inflammation and oxidative stress to sympathetic drive remain poorly understood, and the underlying cellular and molecular targets have yet to be examined. ANG II has been shown to enhance Toll-like receptor (TLR)4-mediated signaling on microglia. Thus, in the present study, we aimed to determine whether ANG II-mediated activation of microglial TLR4 signaling is a key molecular target initiating local oxidative stress in the PVN. We found TLR4 and ANG II type 1 (AT1) receptor mRNA expression in hypothalamic microglia, providing molecular evidence for the potential interaction between these two receptors. In hypothalamic slices, ANG II induced microglial activation within the PVN (∼65% increase, P < 0.001), an effect that was blunted in the absence of functional TLR4. ANG II increased ROS production, as indicated by dihydroethidium fluorescence, within the PVN of rats and mice (P < 0.0001 in both cases), effects that were also dependent on the presence of functional TLR4. The microglial inhibitor minocycline attenuated ANG II-mediated ROS production, yet ANG II effects persisted in PVN single-minded 1-AT1a knockout mice, supporting the contribution of a non-neuronal source (likely microglia) to ANG II-driven ROS production in the PVN. Taken together, these results support functional interactions between AT1 receptors and TLR4 in mediating ANG II-dependent microglial activation and oxidative stress within the PVN. More broadly, our results support a functional interaction between the central renin-angiotensin system and innate immunity in the regulation of neurohumoral outflows from the PVN.


........

Hypertension is a multifactorial disease. Although a number of different underlying mechanisms have been learned from the various experimental models of the disease, hypertension still poses challenges for treatment. Angiotensin II plays an unquestionable role in blood pressure regulation acting through central and peripheral mechanisms. During hypertension, dysregulation of the Renin-Angiotensin System is associated with increased expression of pro-inflammatory cytokines and reactive oxygen species causing kidney damage, endothelial dysfunction, and increase in sympathetic activity, among other damages, eventually leading to decline in organ function. Recent studies have shown that these effects involve both the innate and the adaptive immune response. The contribution of adaptive immune responses involving different lymphocyte populations in various models of hypertension has been extensively studied. However, the involvement of the innate immunity mediating inflammation in hypertension is still not well understood. The innate and adaptive immune systems intimately interact with one another and are essential to an effectively functioning of the immune response; hence, the importance of a better understanding of the underlying mechanisms mediating innate immune system during hypertension. In this review, we aim to discuss mechanisms linking Angiotensin II and the innate immune system, in the pathogenesis of hypertension. The newest research investigating Angiotensin II triggering toll like receptor 4 activation in the kidney, vasculature and central nervous system contributing to hypertension will be discussed. Understanding the role of the innate immune system in the development of hypertension may bring to light new insights necessary to improve hypertension management.


View attachment 30637
Interesting .I posted a thread about endotoxin and vascular dysfunction, that ties in very well to that.
(1 dose of endotoxin causes endothelial dysfunction for up to 1 week)

So that means the spike proteins increase TLR4 through a ACE2-dependant AND ACE2-independent mechanism. Even worse ...
 

youngsinatra

Member
Joined
Feb 3, 2020
Messages
926
Age
23
Location
Frankfurt, Germany
One of the body's defenses against angiotensin and circulatory problems is ACE2. The `virus`, vaccine, antivirals expose the body to spike protein or different stressors that reduces ACE2 and blocks the body's anti-inflammatory and anti-coagulation response. Things that increase ACE2 and reduce AT1 should work.

I took three studies at random.

……….

A renin-angiotensin level that is inappropriately high for the systemic blood pressure and the state of sodium balance is now recognized to be one of the modifiable cardiovascular risk factors. Angiotensin acts both as a circulating hormone and as a locally acting paracrine/autocrine/intracrine factor. The adverse effects of angiotensin on the heart include the mechanical results of elevated resistance to the pumping function of the myocardium, as well as the effects of neurohumoral abnormalities on various cardiac structures. In addition, cardiac damage follows acute ischaemic injury or chronic energy starvation due to coronary artery disease, attributable to either mechanical obstruction (atherosclerotic and/or thrombotic) or functional stenosis (vasospasm). Activation of the renin-angiotensin system has several haemodynamic and humoral consequences, all of which may damage the myocardium. These include acute myocardial ischaemia, left-ventricular hypertrophy, arrhythmias, alterations in the coagulation–fibrinolysis equilibrium, increased oxi- dative stress, and pro-inflammatory activity.

Angiotensin II exerts several direct effects on the heart via activation of the angiotensin type-1 receptor (AT1 receptor)
, which is a G-protein-linked receptor identified on cardiac myocytes that activates protein kinase C through formation of diacylglycerol and hydrolysis of phosphatidylinositol.17,18 The positive inotropic, mitogenic and arrhythmo- genic actions of A II are now well documented.19,20 It stimulates both hypertrophy and hyperplasia of cardiac myocytes as well as vascular smooth-muscle cells by activating proto-oncogenes, which is one of the early steps in cell hypertrophy and division. Intracellular second messengers generated by stimulation of AT1 receptors, such as phospholipases and phosphatidic acid, are now known to enhance mitogenesis; they were shown to increase thymidine incorporation in various cells,21,22 and induce mRNA expression of c-fos and c-myc.23 In fact, a close correlation has been reported in experimental animals between LVH and myocardial levels of A II.24 In addition to its direct action of stimulating protein synthesis and cell proliferation, A II has also been shown to release other growth factors from smooth-muscle cells and blood cells, such as the platelet-derived growth factor. Furthermore, it enhances peripheral sympathetic activity and exerts a permissive action on the release of noradrenaline,25 which possesses trophic properties of its own and promotes myocardial cell growth and hypertrophy.26

In addition to vasoconstriction-induced myocardial ischaemia, A II promotes myocardial damage by affecting normal oxygen metabolism. This exerts both direct deleterious effects on myocardial (and other) cells, and indirect effects via enhanced lipid peroxidation and atherogenesis leading to coronary artery disease.


Angiotensin II causes increased activity of the NADH and NADPH oxidases, with production of large amounts of superoxide anions.30 The data suggest that reactive oxygen intermediates may be part of the normal intracellular signalling responses following stimulation of AT1 receptors. Reactive oxygen species are known to cause oxidative damage to various cellular structures, including membranes, proteins such as intracellular enzymes, DNA sequences and DNA repair enzymes.31 Acute myocardial infarction is accompanied by activation of numerous systemic and local neurohumoral factors, including the renin-angiotensin system.32,33 Furthermore, reperfusion of the acutely infarcted area (as obtained experimentally by removal of a coronary ligature and clinically by thrombolytic agents) produces a surge in reactive oxygen species, causing tissue damage beyond that inflicted by ischaemia34 and partially attributed to activation of local humoral factors, including A II.

Another type of oxidative damage that is relevant to coronary heart disease is lipid peroxidation, which is the auto-oxidation of polyunsaturated fatty acid chains of lipids.37 Recent evidence indicates that low-density lipoprotein (LDL) cholesterol has to be oxidized before it becomes atherogenic, and that lipid peroxidation is the first step in this process. Oxidized LDL is taken up by macrophages, stimulates monocyte adhesion to the endothelium, inhibits vasodilation and is generally cytotoxic.38 Recent clinical work suggests that LDL cholesterol derived from hypertensive patients has an increased susceptibility to lipid peroxidation, which the authors attributed to A II


This mechanism would partly explain the increased tendency of hypertensive patients to develop atherosclerotic changes, leading to coronary obstruction as well as peripheral vascular obstructive disease. In fact, there is epidemiological evidence to suggest that high-renin-hypertensive patients are significantly more prone to heart attacks40,41 and to coronary disease in general.

Normal blood rheology depends on the constant equilibrium between forces that enhance intravascular coagulation and intrinsic thrombolytic factors. Disturbance of this process, by inhibitors of the tissue-type plasminogen activator (t-PA), for example, will tilt the balance towards increased thrombogenesis.47 In fact, elevated levels of the PA inhibitor-1 (PAI-1) have been implicated in the pathogenesis of thromboembolic diseases in general,48 and are considered to be a risk factor and/or marker for recurrence of myocardial infarction.49 Angiotensin II was reported to induce secretion of PAI-1 from cultured cells in vitro.50

In vivo infusions of A II in both hypertensive patients and normotensive control subjects were found to induce a rapid dose-dependent increase in circulating levels of PAI-1.51 The finding that A II enhances endothelial synthesis and secretion of PAI-1 suggests an additional mechanism by which activation of the renin-angiotensin system may increase the risk of coronary events. These data are consistent with the epidemiological studies linking high-renin hypertension to increased risk of heart attack, as mentioned earlier.40,41

Angiotensin II as a cardiovascular risk factor - Journal of Human Hypertension

…………….

Summary

There is an increased number of in vitro evidence that angioten-sin II (Ang II) may promote thrombosis. However there are no in vivo experiments exploring the effect of Ang II on thrombus formation. In the present study we have investigated the influence of Ang II on venous thrombosis in renovascular hypertensive rats. Furthermore, we examined the role of AT1 receptor and Ang II metabolites: angiotensin III (Ang III) and angioten-sin IV (Ang IV) in the mechanisms of Ang II action. The contribution of coagulation and fibrinolytic systems in the mode of Ang II action was also determined. Venous thrombosis was induced by ligation of vena cava. Ang II infused into rats developing venous thrombosis caused dose-dependent increase in thrombus weight, which was partially reversed by losartan, selective AT1 antagonist. Ang III did not influence the thrombus formation in hypertensive rats, while Ang IV caused a marked increase in thrombus weight only in one of the used doses. Our study shows that Ang II via AT1 receptor enhances thrombosis development. The prothrombotic effect of Ang II may partially depend on enhanced leukocytes adhesion to endothelial cells accompanied by accelerated fibrin formation and increased plasma level of PAI-1. Moreover, Ang II action is partially mediated by one of its metabolites – Ang IV.

Thieme E-Journals - Thrombosis and Haemostasis / Abstract

………..

The monocarboxypeptidase, ACE2, which is predominantly expressed in the heart and kidneys shuttles angiotensin metabolism away from the formation of Ang II thereby functioning essentially as a negative regulator of the RAS [2]. In human heart failure, there is upregulation of ACE2 which may provide a key adaptive and cardioprotective mechanism [7–9]. Our current study shows that in the absence of ACE2, cumulative damage from Ang II acting via the AT1 receptors is the predominant cause of the age-dependent cardiomyopathy. The phenotypic alterations in our mouse models closely mimic the biochemical, structural and functional alterations in human heart failure. The AT1 receptor blocker, irbesartan, slowed the progression to heart failure in Ace2−/y mutant mice which is consistent with the use of AT1 receptor blockers as effective therapy for human heart failure. Consistent with the increased oxidative stress in the myocardium, loss of ACE2 also leads to Ang II-dependent renal oxidative damage and glomerular injury [6] which together with possible vascular injury may in part contribute to the overall age-dependent cardiomyopathy in ACE2 null mice.

We have shown that in aged Ace2−/y mice, increased Ang II action via AT1 receptors was associated with enhanced pathological hypertrophy, ventricular dilation and compromised systolic function. Ang II can induce reactive oxygen species such as H2O2 (hydrogen peroxide) and O2− (superoxide) formation via activation of NADPH oxidase [3,20,21,40,41]. Ang II-mediated activation of the NADPH oxidase complex via AT1 receptors has been well documented in cardiomyocytes, vascular and endothelial cells [17,21,40]. Reactive oxygen species interact with nitric oxide which may deplete endogenous nitric oxide [42] while also leading to the formation of reactive and toxic species such as peroxynitrite (ONOO−) [3,21,40]. NADPH oxidase activity is increased in human heart failure which may facilitate the negative inotropic effects of Ang II [41,43]. We observed a marked increase in Ang II-dependent infiltration of neutrophils into the myocardium in ACE2-deficient hearts which was markedly reduced by AT1 receptor blockade. Ang II mediates a wide variety of cardiac inflammatory processes and leads to an upregulation of proinflammatory markers [22,23,44]. Ang II-mediated recruitment and activation of neutrophils perpetuate the free radical induced myocardial injury [20,45] and increase collagenase activity via the induction of MMP-8 expression which can degrade the extracellular matrix thereby compromising systolic function [18]. The activation of MAPK pathways is a characteristic finding in heart disease and plays a key role in the progression to heart failure [24]. Our data confirms the activation of myocardial MAPK pathways in aged Ace2−/y mutant mice and is consistent with changes observed following pressure-overload in young Ace2−/y mutant mice [19]. Indeed, ERK1/2, JNK1/2 and p38 pathways were all activated in Ace2−/y mutant mice and while AT1 blockade maintained the phosphorylation of the adaptive ERK1/2, activation of the maladaptive, JNK1/2 and p38, was selectively reduced.

Angiotensin II-mediated oxidative stress and inflammation mediate the age-dependent cardiomyopathy in ACE2 null mice
„Furthermore, the role of vitamin D has been highlighted in regulating the immune system of the body through renin-angiotensin-aldosterone system (RAAS) inhibition, by downregulating host cell receptor expression to prevent virus attachment. Besides, vitamin D also acts through several other mechanisms like upregulating antimicrobial peptides, fighting against the proinflammatory milieu created by the invading virus, and interfering with the viral replication cycle as well as calcitriol-mediated blockage of CREB protein. Hypovitaminosis D is attributed to elevated risks of acute respiratory distress syndrome (ARDS), lung damage, and cardiovascular disorders, further increasing the severity of COVID-19 infection.“
Role of ACE 2 and Vitamin D: The Two Players in Global Fight against COVID-19 Pandemic

I think in sufficient amounts vitamin D is truely miraculously working on the RAAS. I know relatives whose high blood pressure completely resolved with higher dose vitamin D. (10-20’000 IU/d)
Probably doing good things, because of it‘s modulatory effects on RAAS, PTH, angiotensin and so on.
 

Daniil

Member
Joined
Feb 13, 2021
Messages
713
Location
Moscow
What other things (besides progesterone, vitamin E and Aspirin) thin the blood? I would like to take something blood thinning to prevent covid, but I already have a fairly low iron level and I don't want to lower it more with the above supplements. And I don't want my mouth to stink of garlic.
 

StephanF

Member
Joined
Jul 8, 2014
Messages
462
Location
Reno
In your view, would Zeta Aid cure Afib?
I am not a doctor! I read Dr. T.C. McDaniel's book 'Disease Reprieve', in his mid 50s, he suffered from severe PVC (premature ventricular contraction) and was upset that, as he wrote, they put people on the moon but couldn't treat his PVC. Until he stumbled upon the work by Thomas M. Riddick and the connection between cardiovascular disease and the Zeta Potential. He applied Riddick's recipe, modified it a bit, and 'cured' his PVC, meaning as long as he took this supplement, he was ok. He lived to almost 102 years, didn't suffer from Parkinson's or Alzheimer's, the same with the siblings that follow his advice. I talked to his daughter Marybeth a week ago, she told me that her father's father died in his 50s from a heart attack and that a sister of her father lived to 105 years! So he was doing something right.

Whether that applies also to your condition, I don't know, but Zeta Aid is just a mix of beneficial, potassium-based electrolytes, it is not harmful, so you could try it out but ask your doctor first, especially for the potassium content, I am not sure if that is contra-indicated for your condition. The amount of potassium in a single serving of Zeta Aid is approximately 150 mg (I don't know the exact recipe), or less than 0.5 g per day (for three servings). That is the amount in one half of an avocado or one banana.

Then my personal opinion is that heart disease stems from bacteria, probably from the mouth (gum disease or root canal issues), maybe also from the gut. These bacteria form 'biofilms', a slimy film in which they breed and which the lymphocytes can't get to. This causes inflammation of the arteries or destruction of the heart valves (happened to a friend of mine who couldn't afford routine dental cleaning). If the Zeta Potential of the blood is strong, this can't happen, the increased electrical repulsion will not allow for the bacteria to attach themselves to the arterial walls, or if there were any, the increased Zeta Potential will dissolve them.

I also think that MMS (chlorine dioxide) will help here. It is a gas that can penetrate those biofilms and kill the bacteria. I have witnessed the complete remission of arthritis in the caretaker of my mom in 2012, she had two stiff fingers on her right hand. She took four activated drops once a day and after only 5 days, the arthritis was gone. Again, I think this is due to bacteria from the mouth. Root canal treated teeth can harbor bacteria in the millions of micron-size channels of the dentin, the softer tooth material underneath the enamel. Then my wife, when she lived in Japan, she had a root infection and a stomach ulcer. I looked it up and found a medical review article, where publications were cited and summarized that an infected root can be a 'reservoir of h-pylori' that can re-infect a stomach ulcer. So here you have to treat the ulcer AND the infected tooth!

Then my mom had also a stomach ulcer in 2013, she was admitted to the hospital, she received a blood transfusion, then had two severe strokes and died. Both, Dr. T.C. McDaniel and Thomas M. Riddick warned about blood transfusion. If the Zeta Potential is weak, then blood clots will form, leading to heart attack, stroke or lung embolism. My elder brother also died of the consequences of blood transfusions during an 11-hour long bladder operation. I handed out a pamphlet about the Zeta Potential to all the doctors there, they never heard about it! It is not taught in medical school.
 
Last edited:
Similar threads
Thread starter Title Forum Replies Date
G Vitamins/Minerals One Needs To Supplement On a "Peat" Diet? Ask For Help or Advice 25
L Recommended daily doses of vitamins and minerals according to Ray peat Ask For Help or Advice 18
Hans Here’s how to get all your vitamins and minerals without vegetables Articles & Scientific Studies 22
S Rosacea, Psoriasis, seb dermatitis, eczema, what vitamins and minerals are lacking if you have those? Skin 37
Amazoniac Handbook Of Vitamins, Minerals And Hormones - Roman J. Kutsky Book Recommendations 6
N Do B Vitamins Deplete Any Other Vitamins Or Minerals? Ask For Help or Advice 7
R Question About Kirkland Signature Daily Multi Vitamins And Minerals Supplements 2
R Test For Vitamins, Minerals, Amino Acids: Blood Work, Labs 0
B Am I Missing Out On Any Vitamins And Minerals, Using Gelatin Instead Of Meat? Gelatin 2
Amazoniac Cravings: vitamins x minerals Diet, Recipes 8
M Most multivitamins have these 2 toxic minerals in them Ask For Help or Advice 2
M Lack of Trace minerals digestion related or not enough in food nowadays? Ask For Help or Advice 4
M Liquid minerals for people who don’t absorb them well? Ask For Help or Advice 6
M Best trace minerals foods? (Boron, molybdenum etc) Diet 7
B Whole blood minerals Blood Work, Labs 10
F Any good place to test your minerals level in the UK? Ask For Help or Advice 0
G How would you say these serum levels of minerals look like? Minerals 0
cinderella Minerals, Oxidisers And Hair Hair & Nails 2
Nuri55 Is It Peat Friendly To Take Minerals In The Form Of Powder? Minerals 0
R Light And Minerals Red Light, Infrared, LLLT 0
Beefcake Boiling A Few Drops Of Concentrace Minerals Drops Experiments 1
Fractality Does AC Prevent Macronutrients/minerals From Being Assimilated? Activated Charcoal 1
G How Does Sugar "Chelate Minerals" Sugar, Honey 12
Fractality Other Minerals To Balance A Higher Than Normal Calcium Intake? Ask For Help or Advice 6
M Depleted Minerals In Soil- Is It Impossible To Get Enough Nutrients Without Supplementing? Macros & Micros 6
Captain_Coconut Alkaline Minerals, Growth Hormone, Morning Pain, What To Do? Ask For Help or Advice 0
TubZy What Is Everyone Doing For Minerals? Supplements, Pharmaceutical Drugs 25
P Bone Broth Analysis, Minerals Articles & Scientific Studies 5
Richiebogie Insufficient sodium leads to loss of other minerals... Ray Peat Quotes 0
YuraCZ Minerals.. How Much Is Too Much? Diet 1
P Timing Of Vitamin C And Minerals C 0
Zachs Megadosing minerals Minerals 22
lindsay Understanding Alkaline Minerals. Acidity vs. Alkalinity 7
F Running Hot! [alkaline Minerals] Health 5
W Ionic minerals, anyone? Minerals 3
G Fruit vs Refined Sugar (Minerals, Potassium, OJ...) Kmud Interview: Sept.17,2010 - Sugar I [Clipped.In 0
theantagonist EU sources for bulk powder supplements (vitamins)?? Supplements 7
TheSir Water filtration to isolate b-vitamins from a magnesium pill? Ask For Help or Advice 0
D What are the most important vitamins and nutrients for the function of each organ Ask For Help or Advice 3
M Do policosanols and vitamin b1 have any interactions with other nutrients? how does thiamine affect methyl groups, other b vitamins and histamine? Ask For Help or Advice 0
T Saturation b vitamins Vitamins 2
haidut Vitamins D and E - the Taliban in the COVID-19 war Scientific Studies 54
A Sleeping issues and frequent and night urination - too many vitamins a possible culprit? Ask For Help or Advice 7
R What B vitamins do you mega-dose, if any? Water-Soluble Vitamins 2
Mito Serum Vitamins and Homocysteine Levels in OCD Articles & Scientific Studies 0
D Low levels of vitamins B2, B6, B9 in adults with ADHD Mental Issues 2
K Question about added vitamins in milk Milk 2
TheBeard B Vitamins Doubled My Total Testosterone Levels Male Issues 105
H A Cross-sectional Study Of Plasma Trace Elements And Vitamins Content In Androgenetic Alopecia In Me Articles & Scientific Studies 0
sugarbabe Role Of Vitamins A And D In The Pathogenesis Of Influenza: A New Perspective Viruses, Parasites, Fungus, Vaccines 1

Similar threads

Top