Taking Enzymes To Lyse Plaque, BP Rising, WBC, Urinating A Lot-Frustrated

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danishispsychic

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Never had a colonic nor enema but curious about how using garlic in colonics would help. Is it the sulfite in garlic or the allicin in garlic?



I don't know that they're scams but just the same I think their use is limited. The scans only see something in advanced stages, which means it's mostly useful when you're already screwed. I can't rely on it to tell me there's something at initial stages, when you can nip it at the bud. It gives people the wrong impression they're fine when they're not. So my nit is on it giving false negatives, and with this false sense of comfort, they get deeper in disease.

But what you're saying is that it gives false positives, and false positives are just as misleading.
Oh gosh- There was a typo on my post. I would recommend eating garlic . I would not recommend any kind of enema besides coffee and of course water. I would recommend getting gravity colonics in a series of about 12, like 3 a week for a month or 6 weeks. If you want to start with eating raw garlic, that will start killing things, you can do distilled water enemas or just go right into the colonics thing. It can be pricey but if you do a whole series it is a game changer.
 
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yerrag

yerrag

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Oh gosh- There was a typo on my post. I would recommend eating garlic . I would not recommend any kind of enema besides coffee and of course water. I would recommend getting gravity colonics in a series of about 12, like 3 a week for a month or 6 weeks. If you want to start with eating raw garlic, that will start killing things, you can do distilled water enemas or just go right into the colonics thing. It can be pricey but if you do a whole series it is a game changer.
It was a typo? Come to think of it, a garlic colonic wouldn't work. I tried to save my cat once by doing an enema not realizing an enema cannot be acidic. I gave the cat a solution of ascorbic acid. All it did was to cause liquid, mostly water, to flush out. Needless to say, I wasn't able to save the cat. She couldn't take anything orally, and that was why I went the rectal route. Not sure whether the garlic would be acidic, but in sufficient concentration it could be enough acidic given its sulfite content.

I think oral intake of garlic would help. Thanks. Just not too much. I had once tried a lot of it and it ended up acidifying my stem and lowered my immunity. I fell to "the more the better" fallacy not knowing any better. Now, I know the poison is in the dosage.
 
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yerrag

yerrag

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Thanks for the links. Very helpful in understanding the role of inflammation, especially as it pertains to a favorite subject of Ray Peat - endotoxins.

I spent a good part of the weekend ransacking my brains trying to make sense of the seeming helplessness of fixing my hypertensive condition. The more I dig in to the causes, the deeper I get into it, and the more I realize that I'm in my own personal quagmire. The saving grace here is that I've become more familiar with where ground zero is, and what the offending culprits are. It also helps knowing to separate the secondary and even the tertiary cause and effect relationships from the primary cause of my high blood pressure. It's also gratifying to know that, as complicated as it is to extract myself from this booby-trapped Vietnam War jungle, it still isn't so bad given that I have allowed my body free reign to adapt to the situation. I've not fallen prey to the scourge of intervention from pharma and its doctors, attendant with side effects that would have systemic repercussions on my health.

Endotoxins form the front and center of my condition. It was endotoxins that made my teeth subject to many cavities. I had eleven cavities, all patched by mercury fillings, which is the subject of another episode of healing). The same endotoxins were to attach to my teeth, to allow bacteria to penetrate my gum line, and to lead to periodontal infection. This was a worse condition to have, as the infection was beyond detection, and it lay latent for at least fifteen years. During this time, I developed hypertension, and it wasn't discovered until last year, when two of my teeth loosened, revealing the infection. With this much time for endotoxins to work its dark magic, and my body to make adaptations the best way it can, I can only hope I can still undo the changes wrought on my body.

The endotoxins would affect my kidneys first, which would be expressed as hypertension. Over fifteen years, the hypertension would worsen, going as high as 240/120. Although the hypertensive condition has subsided to 180/120 from half-effective measures, much work remains. Even though the initial cause, periodontitis, is gone, the effects in the form of vascular plaque persist. In this plaque, dormant bacteria and accumulated endotoxins remain. It would continue to release bacteria and endotoxins (as slowly as calcium would be leached from limestone in water), or quickly, such as when I would use systemic enzymes to cause plaque to be lysed.

It was with my generous use (for one week only) of Serrapeptidase that I would connect the dots, and make the conclusion that I have an endogenous store of bacteria and endotoxins, in the plaque that lines my vascular system. The first indication was that the 3x120,000 daily dose of Serraptidase would cause me to urinate heavily (urination every 45 minutes during the day, with a bladder full, and at night, waking up 4-5x to pee). When I got my blood test results, where wbc and neutrophils shot up, it made me realize what was happening. There was increase in inflammation, and it was because there was a flood of bacteria and endotoxins.

I stopped taking the enzymes, and began to take doxycycline. My wbc and neutrophils level went down, and my urination went back to normal. Not only that, at a certain point my urination stopped being foamy. Foamy urine was something I've resigned myself to, and I attributed it to microalbuminuria (micro because it wasn't so bad to be considered albuminuria). To see the foam disappear piqued my interest. I soon arrived at a theory, that endotoxin was being bound by albumin into a complex, and what this was doing has these effects: 1) it lowers my serum albumin levels (currently staying at 42, optimal range at 40-50, not bad but can be better); 2) the complex may likely be easily excreted thru urine and cause the foaming, as well as lower my serum albumin; 3) lowered serum albumin lowers the transport of substrates and nutrients as well as waste products of metabolism, and could lower my metabolic rate; and just as importantly, it could cause hypovolemia (lower blood volume) as albumin and sodium form a complex, and this complex increases the osmolar concentration of plasma, and this attracts water from the extracellular space into plasma, thereby increasing blood volume. With lower albumin, less blood volume would result. Here are two articles I reference discussing albumin: When energy fails: Edema, heart failure, hypertension, sarcopenia, etc. and VetFolio:

sodium also has a direct effect that tends to prevent the leakage of water and albumin out of the blood vessels, helping to maintain the blood volume which is needed to perfuse the kidneys, preventing them from producing signals to increase blood pressure and aldosterone. There is a large amount of albumin in the blood serum, and sodium ions associate with the negative electrical charges on the albumin molecule. This association causes the complex of albumin and sodium to attract a large amount of water, that is to exert osmotic or oncotic pressure. This oncotic pressure causes any excess extracellular water to be attracted into the blood vessels, preventing edema while maintaining the blood volume (from first reference)

Albumin molecules, which are highly soluble in water, carry many charged amino acid residues, resulting in a net charge of -17 at a normal physiologic pH.3 This creates a strong attraction of sodium ions and other cations around its core structure. Water is also pulled into the vasculature as a result of the sodium attraction to albumin. Each gram of albumin is capable of holding 18 ml of water within the intravascular space; this explains why albumin alone contributes to approximately 80% of plasma COP.2 During times of stress, acute loss, or decreased synthesis of albumin, there is a rapid equilibration of extravascular and intravascular albumin to maintain COP (second reference).

The above paragraph may explain why my urine foams, and why I'm excreting albumin in my urine, and this would be an indication that I have a kidney problem, as a healthy kidney should not be allowing albumin to be excreted. But this isn't enough proof of an ailing set of kidneys, given that the kidneys aren't really excreting albumin, but really albumin complexed with endotoxin (but I'm just speculating here). But it's more a matter of association than direct proof that's at work here. Endotoxin complexing with albumin is just one side of the coin, endotoxin also causes amyloid protein to be formed in the kidneys, and then this impairs the filtering efficiency of the kidneys. So I can say that when the kidneys are excreting albumin through urine, it's just as likely that the kidneys are not filtering as efficiently as it could, because those two effects are intertwined, with endotoxins manifesting its effects in two different ways in the kidneys.

Which is why I'm beginning to see my above-normal urine albumin-creatinine ratio, my low-end-of-optimal range serum albumin, and my high serum creatinine (indicative of low glomerular filtration rate) as all tied in together with the effect of endotoxins. I've discussed the mechanism by which endotoxins relate to albumin in my urine, but now I'll bring its effect on the filtration rate by referring to this wikipedia piece on amyloidosis : Amyloidosis - Wikipedia

Amyloidosis is a group of diseases in which abnormal proteins, known as amyloid fibrils, build up in tissue...

...The four most common types of systemic disease are light chain (AL), inflammation (AA), dialysis (Aβ2M), and hereditary and old age (ATTR).

...Amyloid deposition in the kidneys can cause nephrotic syndrome, which results from a reduction in the kidney's ability to filter and hold on to proteins. The nephrotic syndrome occurs with or without elevations in creatinine and blood urea concentration,[6] two biochemical markers of kidney injury. In AA amyloidosis, the kidneys are involved in 91–96% of people,[7] symptoms ranging from protein in the urine to nephrotic syndrome and rarely chronic kidney disease.

...AA amyloidosis usually spares the heart.

...AA is suspected on clinical grounds in individuals with longstanding infections or inflammatory diseases.
The description I lifted from wikipedia fits my condition to a tee. My kidney condition is the tye where creatinine is slightly elevated but the BUN isn't. There is some protein in the urine and I am just borderline CKD.

Based on the above, I believe that it's the endotoxins that have led to the amyloid formation in the glomerulus of my kidneys, leading to reduced kidney filtation rates; and that it's also the endotoxins that are are causing increased urination as well as foam in the urine. It is the endotoxins and its effects that is causing my high blood pressure as well, given that the amyloid plaque deposits block the flow in the capillaries.

Given what I know now about my condition, where my kidney's glomeruli's function is impeded by amyloid plaques caused by endotoxins, and where continued exposure to endotoxins continue to be a source of inflammation as well as the cause of low serum albumin, my effort now should be directed towards:slowly clearing the glomerular capillaries of obstruction to restore blood flow and optimal kidney filtration, by a long-term process of controlled lysing of amyloid plaque using a suitable dosage of serrapeptase that will release a limited amount of bacteria and endotoxins from the plaque, such that the amount will be ably neutralized by both the innate immune system and supplements that would destroy the bacteria and deactivate the endotoxins as well as blunt the inflammatory response (TLR4 and CD14).

It took 15 years to get to this point, and I hope it won't take as much time to restore my kidneys back to where it was, and as a result, to see my blood pressure get back to normal.
 
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I thought you had taken antibiotics a few months ago. Did you stop? Are you restarting?

And have you tried high dosages of vitamin K2 MK4 along with good high levels of dietary calcium?
 
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yerrag

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I thought you had taken antibiotics a few months ago. Did you stop? Are you restarting?

And have you tried high dosages of vitamin K2 MK4 along with good high levels of dietary calcium?

I took doxycycline on and off, for different reasons. Took it to ease the load on my innate immune response, to keep wbc and neutrophils down - as I believe when they're high there's also high inflammation and this leads to higher blood pressure as well as lower metabolism (due to exhaustion of NADPH as well as anti-oxidant stores). I took it off when I've been using doxycycline for too long, to keep from bacteria developing a resistance to doxy. I also tried using other antibacterials when not using doxy - such as colloidal silver, and oregano essential oil in VCO base. Now, I'm restarting doxy in order to clean up on the bacteria and endotoxins released from the recent use of serrapeptase, which I've kept low (as my 3 x 120,000 spu daily usage precipitated a bacteria and endotoxin ***t storm causing me to start this thread).

I've been using 15 mg k2, not a high dose. But my calcium intake could have been higher.
 
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yerrag

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I stopped taking the enzymes, and began to take doxycycline. My wbc and neutrophils level went down, and my urination went back to normal. Not only that, at a certain point my urination stopped being foamy. Foamy urine was something I've resigned myself to, and I attributed it to microalbuminuria (micro because it wasn't so bad to be considered albuminuria). To see the foam disappear piqued my interest. I soon arrived at a theory, that endotoxin was being bound by albumin into a complex, and what this was doing has these effects: 1) it lowers my serum albumin levels (currently staying at 42, optimal range at 40-50, not bad but can be better); 2) the complex may likely be easily excreted thru urine and cause the foaming, as well as lower my serum albumin; 3) lowered serum albumin lowers the transport of substrates and nutrients as well as waste products of metabolism, and could lower my metabolic rate; and just as importantly, it could cause hypovolemia (lower blood volume) as albumin and sodium form a complex, and this complex increases the osmolar concentration of plasma, and this attracts water from the extracellular space into plasma, thereby increasing blood volume. With lower albumin, less blood volume would result. Here are two articles I reference discussing albumin: When energy fails: Edema, heart failure, hypertension, sarcopenia, etc. and VetFolio:

sodium also has a direct effect that tends to prevent the leakage of water and albumin out of the blood vessels, helping to maintain the blood volume which is needed to perfuse the kidneys, preventing them from producing signals to increase blood pressure and aldosterone. There is a large amount of albumin in the blood serum, and sodium ions associate with the negative electrical charges on the albumin molecule. This association causes the complex of albumin and sodium to attract a large amount of water, that is to exert osmotic or oncotic pressure. This oncotic pressure causes any excess extracellular water to be attracted into the blood vessels, preventing edema while maintaining the blood volume (from first reference)

Albumin molecules, which are highly soluble in water, carry many charged amino acid residues, resulting in a net charge of -17 at a normal physiologic pH.3 This creates a strong attraction of sodium ions and other cations around its core structure. Water is also pulled into the vasculature as a result of the sodium attraction to albumin. Each gram of albumin is capable of holding 18 ml of water within the intravascular space; this explains why albumin alone contributes to approximately 80% of plasma COP.2 During times of stress, acute loss, or decreased synthesis of albumin, there is a rapid equilibration of extravascular and intravascular albumin to maintain COP (second reference).

The above paragraph may explain why my urine foams, and why I'm excreting albumin in my urine, and this would be an indication that I have a kidney problem, as a healthy kidney should not be allowing albumin to be excreted. But this isn't enough proof of an ailing set of kidneys, given that the kidneys aren't really excreting albumin, but really albumin complexed with endotoxin (but I'm just speculating here).

In Serum albumin - Wikipedia :

Albumin (when ionized in water at pH 7.4, as found in the body) is negatively charged. The glomerular basement membrane is also negatively charged in the body; some studies suggest that this prevents the filtration of albumin in the urine. According to this theory, that charge plays a major role in the selective exclusion of albumin from the glomerular filtrate. A defect in this property results in nephrotic syndrome leading to albumin loss in the urine.
So, if albumin complexed with LPS changes the electrical charge of the albumin to becoming positively charged, it could very well cause it to be excreted to urine. I wonder if there's been a study done that analyzes the albumin excreted in urine, as to whether it's albumin or an albumin complex.

Which is why I'm beginning to see my above-normal urine albumin-creatinine ratio, my low-end-of-optimal range serum albumin, and my high serum creatinine (indicative of low glomerular filtration rate) as all tied in together with the effect of endotoxins.

The standard of care (which conventional doctors use) range of albumin is 3.5 -5.0 g/dL, while that of Dr. Weatherby is 4.0-5.0. While I'm at 4.2, it's small comfort. Or actually, no comfort at all. In https://www.renalandurologynews.com...y-failure-associated-with-low-albumin-levels/ :

In a study of community-dwelling adults, ESRD was 61% and 69% more likely to develop among individuals with serum albumin levels in the first and second quartiles (below 4.0 and 4.0–4.1 g/dL), respectively, compared with those who had levels in the fourth quartile (4.4 g/dL or higher) in a fully adjusted model, Carl P. Walther, MD, of the Baylor College of Medicine in Houston, and colleagues reported online ahead of print in Nephrology Dialysis Transplantation. Each 0.33 g/dL decrease in serum albumin was associated with a 16% increased risk of ESRD.

I really have to do something that will result in my serum albumin going up then. I really suspect that my albumin is being used up in complexing with endotoxin in order to neutralize it and pave for the endotoxin to be excreted by the liver thru bile and through the fecal route. The albumin actually becomes part of the LBP (lps binding protein).

Everything I've observed seems to be making more sense now. The increased urination and the increased foam when I urinate and how it relates to increased serum endotoxin levels, especially when the the large amount of serrapeptidase enzymes I took caused a large amount of LPS to be lysed and released from plaque into the bloodstream. I now know why my serum albumin cannot go any higher, and why at this lower level of serum albumin I could not increase my plasma volume. It's because with lower serum albumin, not enough sodium ions can be attracted to form a sodium-albumin complex, and with lower sodium the plasma pool, not enough water can be attracted from the interstitial space to form a larger plasma volume. With a lower blood volume, my blood pressure has to be increased.

Ray Peat, in Salt, energy, metabolic rate, and longevity has also stated:

Bacterial endotoxin, and other things that cause excessive capillary permeability, edema, or shock-like symptoms, will activate renin secretion.
The next and obvious thing for me is to focus my efforts on containing further damage to my kidneys by doing everything to manage the existing store of endotoxins in my vascular system, residing and slowly being released by plaque. I can't just scrape the plaque off my blood vessels, nor can I lyse it off in one fell swoop. I can either let it naturally slough off and then have enough substances available to curtail its effect, without having it to bind with my serum albumin. Though this would mean I would have to accept the plaque I have as a necessary evil.

Now, on to continuing research on endotoxins and the substances that will do an effective job of countering its effects.

 
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Fish! I had to post these here because I was about to lose them. Hopefully you find something useful.

- Natural Products with Toll-Like Receptor 4 Antagonist Activity

"One of the advantages of innate immune receptors is that they had evolved by natural selection to recognize a few highly conserved structures shared by large groups of microorganisms (Table 1). For instance, all gram-negative bacteria have lipopolysaccharides (LPS); therefore, the lipopolysaccharide pattern recognition receptor of the host (e.g., TLR4) can detect the presence of virtually any gram-negative bacterial infection [4]. Indeed, it has been demonstrated that some TLRs, and particularly TLR4, respond to danger-associated molecular patterns (DAMPs) that are endogenous molecules of the host, released by injured tissue and dying cells [5] (Table 1). The stimulation of TLRs by the corresponding PAMP or DAMP initiates intracellular signaling cascades leading to the activation of transcription factors, such as AP-1, NF-kB, and interferon regulatory factors (IRFs) [6]. Signaling by TLRs results in a variety of cellular responses including the production of proinflammatory cytokines, type I interferons (IFNs), and effector cytokines that direct both innate and adaptive immune responses [7]."

"Although TLR-mediated signaling has a leading role in both eradicating microbial infections and promoting tissue repair, the regulation must be tight. TLRs are implicated in a number of infectious and noninfectious diseases and immune disorders, as well as in cancer; they can either promote or inhibit disease progression [4, 8–11]. The importance of TLRs triggering in infectious diseases is evident, as they are the main receptors of innate immunity involved in sensing bacterial, fungal, and viral infections; indeed, it has been recently demonstrated that TLRs, and particularly TLR4, are involved in noninfectious diseases [reviewed in [4]]. TLR4 engagement by endogenous ligands has been demonstrated to directly contribute to the process of ischemia/reperfusion injury. Furthermore, in neuroinflammation, which is the common hallmark of several neurodegenerative and neurological diseases, TLR4 has been demonstrated to represent a critical amplifier of the proinflammatory response [4, 12]. In experimental models of systemic lupus erythematosus, TLR7 and TLR9 have been shown to play important roles in the production of pathogenic autoantibodies and/or in the development of clinical signs of autoimmunity [8]. TLRs are also expressed on tumor cells, where they may influence tumor growth and host immune responses [13]. It has been demonstrated that melanoma cells express TLR4, and this expression is particularly high in metastatic cells [9]. Triggering of TLR4 on tumor cells by LPS induces the release of several mediators that can favor tumor cell resistance to cytotoxic lymphocytes, reduces apoptosis, and increases invasiveness [9, 13]. TLR targeting could represent a means to regulate the immune response; however, therapeutic agents must be able to antagonize the harmful effects of TLR engagement, without affecting host defense functions."

"Sulforaphane (SFN) [1-isothiocyanato-4-(methylsulfinyl)butane] is a natural occurring compound found in cruciferous vegetables. The chemical structure is reported in Figure 5(b). It has been demonstrated that SFN exerts anti-inflammatory effects by reducing the production of proinflammatory mediators, such as TNF-a, inducible NO synthase, cyclooxygenase-2, and HMGB1 secretion induced by LPS in macrophages [60, 61]."

"Xanthohumol (XN) is a chalcone-type flavonoid of Humulus lupulus (Figure 5(c)) showing anti-inflammatory effects [65, 66]. The anti-inflammatory action was observed on different stimulation pathways, such as those mediated by LPS and IFN-y, in murine and human macrophages [65, 66]."

"Celastrol is a pentacyclic triterpenoid (Figure 5(d)) isolated from the root extract of Tripterygium wilfordii Hook F., used in traditional Chinese medicine to treat various inflammatory and autoimmune diseases, such as rheumatoid arthritis [69–71]. Celastrol has been demonstrated to form covalent Michael adducts with cysteine residues [69]. Based on this nonselective activity, among the different targets of celastrol, there is also MD-2 [27, 71, 72]."​

- Recent clinical trends in Toll-like receptor targeting therapeutics

"Sepsis is the worst outcome of host-pathogen interaction and is the leading cause of death in United States.[53,54] The infection by Gram-positive and Gram-negative bacteria equally contribute to the development of sepsis where exaggerated immune response lead to multiorgan failure and septic shock.[55] These bacteria harbor ligands that trigger TLR2 and TLR4; particularly, the presence of LPS significantly contributes into sepsis development. The septic shock is due to the body immune response rather than infection itself.[56] For sepsis management, various TLR inhibitors are evaluated clinically, and new modalities are being devised recently.[57]"

"TLRs may antagonize one another under certain physiological conditions. For example, TLR2 and TLR9 antagonize each other in a mouse model for oral infection with Salmonella enterica.[151] TLR9 deficiency is manifested as reduced survival, exaggerated cytokine responses, and salmonella hepatitis, while TLR2 deficiency produces the opposite effects. Deficiency of either TLR may disrupt NK cell cytotoxicity, and IFN-y and ROS production.[151]"

"Synergism is very common in TLRs. When monocyte-derived DCs have been triggered with a TLR8 ligand, TLR3 or TLR4 are also activated, resulting in expression of IL-6, IL-10, IL-12, and TNF-a elevation. These results were also confirmed by increased binding of IRF and signal transducers and activators of transcription (STAT) transcription factors to their respective DNA binding sites, which was abolished when NF-kB, p38, and phosphoinositide 3-kinase (PI3K) inhibitors were used.152 These data suggest that co-operation among TLRs is perpetuated, not only at the top level but also among different signaling pathways to ensure proper and balanced expressions of target genes."

"Synergy and tolerance of TLRs are long-established and are critical to the innate immune response. The coadministration of LPS (TLR4 agonist) and MALP-2 (TLR2 agonist) to mouse macrophages resulted in increased TNF-Diokine production.[153] Repeated treatment with LPS or MALP-2 resulted in a hyporesponse, also termed tolerance. Intriguingly, pretreatment with any ligand results in lower responses on exposure to the second ligand.[153] LPS may cause downregulation of the cell surface expression of TLR4 after the second LPS treatment; however, MALP-2- mediated reduction in responses involve modulation of downstream signaling. The acute immune tolerance and cross-tolerance between TLR4 and TLR9 have been studied,[154] indicating that LPS selectively inhibits proinflammatory cytokines, while CpG suppresses both pro- and anti-inflammatory responses. IRAK-M is critical for the induction of this differential response, and its expression is modulated by IL-7.[154]"

"Drug development is a lengthy process that starts with lead molecule identification and progresses through optimization, animal modeling studies, pharmacokinetic and pharmacodynamic studies, and preclinical and clinical stage trials. Therefore, if a drug fails to show any effect or shows toxicity in clinical studies, there must have been a series of oversights during earlier experimental stages. It is hard to give a single reason for any failure and failures may encompass complex issues, such as the use of subjective, composite, or surrogate endpoints.[165] Moreover, biases in outcome reporting and publications; underreporting of adverse events; failure to select an appropriate patient group; preference for relative outcomes, rather than absolute values; no defined core outcome sets; lack of transparency and basic science; inappropriate study population size; and lack of data integrity are among the reasons for trial failures. Finally, during clinical trials involving humans, factors that influence the drug metabolism, distribution, and secretion are diverse that predispose the pharmacokinetically and pharmacodynamically optimized drug molecules to failure."

"Researchers are expending extensive efforts to generate appropriate solutions for various inflammatory, autoimmune, and malignant conditions; however, the process is not straightforward, rather it is littered with unexpected events and outcomes, along with unknown obstructions that severely undermine the efforts of the research community."

"TLRs are among the ideal targets for exploitation in immunotherapy; however, their biology still needs to be better understood in the context of target diseases. These receptors are capable of inhibiting disease pathophysiology, as well as exacerbating inflammatory diseases. Given this dual role, it is imperative to fine tune their activation using a multidrug approach. Cumulative evidence suggests the participation of TLRs in almost all diseases is unique and can be exploited by including their ligands as adjuvant treatment during regular immunotherapy or as part of other therapeutic regimens."​

- Targeting toll-like receptor 4 signalling pathways: can therapeutics pay the toll for hypertension?

"The activation of TLRs by DAMPs plays an inherently protective role, alerting cells to damage for its resolution and repair. However, excessive or prolonged DAMP-mediated stimulation of these innate immune system receptors provokes a chronic inflammatory state that contributes to the maintenance of hypertension (McCarthy et al., 2014). Through intracellular adaptor protein-dependent signal cascades, DAMP-induced TLR activation increases the expression of pro-inflammatory genes (Akira and Takeda, 2004). TLR4 is unique in this sense, being the only TLR known to recruit four adaptor molecules and signal through two distinct pathways to produce pro-inflammatory cytokines and chemokines (Kawai and Akira, 2010). Of particular interest, a variety of cell types that have long-been associated with cardiovascular diseases have been found to express TLR4, such as macrophages, renal epithelial cells, cardiomyocytes, vascular smooth muscle cells (VSMCs), endothelial cells (ECs), glial cells and neurons (Vaure and Liu, 2014). Indeed, a myriad of studies show that abnormal activation of TLR4, primarily by DAMPs, contributes to cardiovascular dysfunction and remodelling, kidney disease and CNS dysregulation. These studies form the basis of the suggestion that DAMP-induced TLR4 stimulation may be the missing link between inflammation and hypertension."

"Table 1 contains a summary of hypertension-related DAMPs that are proposed to modulate TLR4."

"While the influence of TLR4 on BP control is not completely elucidated, TLR4 up-regulation is suggested to contribute to the pathogenesis of hypertension in animal models."

"Aldosterone, the primary human mineralocorticoid, is significantly involved in cardiovascular morbidity and hypertension (Freel and Connell, 2004)."

"[..]increased natriuresis, with a rightward shift in the sodium retention curve, contributes to the maintenance of a hypertensive state."

"TLR4 is expressed in renal epithelial cells, and its overactivation is implicated in the nephropathy associated with various diseases (Zhang et al., 2008; Souza et al., 2015). In the context of the hypertensive kidney, current literature points to AngII as the main mediator of TLR4 activation. In corroboration with this statement, it has been reported that myeloid differentiation factor 2 (MD2)-deficient mice were protected from renal inflammatory injury and fibrosis (Xu et al., 2017). The adaptor protein MD2 is known to play a role in LPS recognition by promoting TLR4–LPS–MD2 complex dimerization (Park et al., 2009). More specifically, Han et al. (2017) have demonstrated that direct hydrogen bond interactions may occur between MD2 and AngII in a manner similar to that of the MD2 and LPS interaction. Based on this evidence, it is reasonable to speculate that AngII could mediate the activation of TLR4 within the kidneys, thereby contributing to inflammation and oxidative stress, both intrinsic factors for the development of end-organ damage in hypertensive patients."

"TLR4-mediated renal damage in hypertension plays a key role in the development and progression of microvascular complications and may represent a new treatment target. Diuretics are one of the main antihypertensive drug classes targeting the kidneys, favouring water and sodium excretion to help relieve tubular pressure and lower BP. However, as AngII is produced systemically, it may continue to activate TLR4 in the face of diuretic therapy, thereby propagating renal microvascular damage. Supporting this notion, combining diuretics with angiotensin converting enzyme (ACE) inhibitors appears to produce better outcomes in hypertensive patients (Ruoff, 1989). A plausible explanation is that inhibiting AngII production may decrease the extent of TLR4 activation, ameliorating renal oxidative stress and inflammation."

"Another cause of renal damage in hypertension comes from the high BP itself, which injures the endothelial layer and contributes to elevated ROS generation. While the precise molecular mechanisms underlying the damage-induced ROS generation are not completely elucidated, recent findings showing an association between increased renal TLR4 activation and worsened outcomes in hypertensive model point to DAMP-mediated TLR4 activation (Pushpakumar et al., 2017). In the kidneys, increased levels of ROS are associated with dysfunctional glomerular and tubular cells (Araujo and Wilcox, 2014). Importantly, as NF-kB is mediated downstream of TLR4 activation and is described as a source of pro-inflammatory cytokines, this may be one mechanism by which TLR4 contributes to renal dysfunction and end-organ damage in hypertension."

"Chronic high BP and shear stress damage the vascular endothelium over time and contribute to the migration and accumulation of both innate and adaptive immune cells in blood vessels (Goulopoulou et al., 2016)."

"The promotion of inflammation is, first and foremost, a beneficial process, protecting against invading pathogens and responding to stress or injury. It is when this initial protective process becomes excessive or chronic that innate immune activation and, specifically, TLR4 signalling, can be calamitous. With overactivation, the disrupted immune homeostasis becomes pathogenic, manifesting as chronic inflammation, such as that observed in hypertension."

"In Figure 2, we present several therapeutic targets known to modulate TLR4 signal transduction, as well as potential targets for future pharmaceutical development. As illustrated, activation of TLR4 triggers two signalling cascades, which ultimately lead to the production of pro-inflammatory cytokines. Based on studies to date, it can be argued that NF-kB is implicated as the principal downstream component, orchestrating aberrant innate immune system activity in hypertension through TLR4. With similar recent findings of NF-kB dysregulation in other inflammation-associated diseases, pharmaceutical constraint of this transcription factor undoubtedly demands further exploration, particularly as a point of target given the multitude of crosstalk within the TLR4 signalling web."

"While not within the scope of this review, it is of note that all TLRs have been shown to induce NF-kB activity upon stimulation, despite their extensive diversity (Singh et al., 2014). Thus, high specificity in an NF-kB governing agent is essential to combatting potential activation of this pro-inflammatory transcription factor either by other TLR pathways or by as of yet undetermined TLR4 mechanisms. On the one hand, our lack of knowledge regarding the extent of TLR4's pathways in hypertension may result in unforeseen complications with putative therapeutics. On the other hand, the potential of supplementary connections could allow for fewer pharmaceutical risks – by targeting the component essential to disease propagation rather than the entire cascade, it is possible that the beneficial effects of TLR4 stimulation will be retained."

"Lastly, it is of critical importance that the potential risks of targeting TLR4 in hypertension be considered. As evidenced by its vast array of ligands, the TLR4 pathway plays a substantial role in shaping the immune response, and the consequences of inhibiting this arm of the immune system are still unclear."

"[..]the potential benefits of targeting TLR4 must be weighed against the risks and disadvantages of immunosuppressant treatment."​
 
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yerrag

yerrag

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Fish! I had to post these here because I was about to lose them. Hopefully you find something useful.

- Natural Products with Toll-Like Receptor 4 Antagonist Activity

"One of the advantages of innate immune receptors is that they had evolved by natural selection to recognize a few highly conserved structures shared by large groups of microorganisms (Table 1). For instance, all gram-negative bacteria have lipopolysaccharides (LPS); therefore, the lipopolysaccharide pattern recognition receptor of the host (e.g., TLR4) can detect the presence of virtually any gram-negative bacterial infection [4]. Indeed, it has been demonstrated that some TLRs, and particularly TLR4, respond to danger-associated molecular patterns (DAMPs) that are endogenous molecules of the host, released by injured tissue and dying cells [5] (Table 1). The stimulation of TLRs by the corresponding PAMP or DAMP initiates intracellular signaling cascades leading to the activation of transcription factors, such as AP-1, NF-kB, and interferon regulatory factors (IRFs) [6]. Signaling by TLRs results in a variety of cellular responses including the production of proinflammatory cytokines, type I interferons (IFNs), and effector cytokines that direct both innate and adaptive immune responses [7]."

"Although TLR-mediated signaling has a leading role in both eradicating microbial infections and promoting tissue repair, the regulation must be tight. TLRs are implicated in a number of infectious and noninfectious diseases and immune disorders, as well as in cancer; they can either promote or inhibit disease progression [4, 8–11]. The importance of TLRs triggering in infectious diseases is evident, as they are the main receptors of innate immunity involved in sensing bacterial, fungal, and viral infections; indeed, it has been recently demonstrated that TLRs, and particularly TLR4, are involved in noninfectious diseases [reviewed in [4]]. TLR4 engagement by endogenous ligands has been demonstrated to directly contribute to the process of ischemia/reperfusion injury. Furthermore, in neuroinflammation, which is the common hallmark of several neurodegenerative and neurological diseases, TLR4 has been demonstrated to represent a critical amplifier of the proinflammatory response [4, 12]. In experimental models of systemic lupus erythematosus, TLR7 and TLR9 have been shown to play important roles in the production of pathogenic autoantibodies and/or in the development of clinical signs of autoimmunity [8]. TLRs are also expressed on tumor cells, where they may influence tumor growth and host immune responses [13]. It has been demonstrated that melanoma cells express TLR4, and this expression is particularly high in metastatic cells [9]. Triggering of TLR4 on tumor cells by LPS induces the release of several mediators that can favor tumor cell resistance to cytotoxic lymphocytes, reduces apoptosis, and increases invasiveness [9, 13]. TLR targeting could represent a means to regulate the immune response; however, therapeutic agents must be able to antagonize the harmful effects of TLR engagement, without affecting host defense functions."

"Sulforaphane (SFN) [1-isothiocyanato-4-(methylsulfinyl)butane] is a natural occurring compound found in cruciferous vegetables. The chemical structure is reported in Figure 5(b). It has been demonstrated that SFN exerts anti-inflammatory effects by reducing the production of proinflammatory mediators, such as TNF-a, inducible NO synthase, cyclooxygenase-2, and HMGB1 secretion induced by LPS in macrophages [60, 61]."

"Xanthohumol (XN) is a chalcone-type flavonoid of Humulus lupulus (Figure 5(c)) showing anti-inflammatory effects [65, 66]. The anti-inflammatory action was observed on different stimulation pathways, such as those mediated by LPS and IFN-y, in murine and human macrophages [65, 66]."

"Celastrol is a pentacyclic triterpenoid (Figure 5(d)) isolated from the root extract of Tripterygium wilfordii Hook F., used in traditional Chinese medicine to treat various inflammatory and autoimmune diseases, such as rheumatoid arthritis [69–71]. Celastrol has been demonstrated to form covalent Michael adducts with cysteine residues [69]. Based on this nonselective activity, among the different targets of celastrol, there is also MD-2 [27, 71, 72]."​

- Recent clinical trends in Toll-like receptor targeting therapeutics

"Sepsis is the worst outcome of host-pathogen interaction and is the leading cause of death in United States.[53,54] The infection by Gram-positive and Gram-negative bacteria equally contribute to the development of sepsis where exaggerated immune response lead to multiorgan failure and septic shock.[55] These bacteria harbor ligands that trigger TLR2 and TLR4; particularly, the presence of LPS significantly contributes into sepsis development. The septic shock is due to the body immune response rather than infection itself.[56] For sepsis management, various TLR inhibitors are evaluated clinically, and new modalities are being devised recently.[57]"

"TLRs may antagonize one another under certain physiological conditions. For example, TLR2 and TLR9 antagonize each other in a mouse model for oral infection with Salmonella enterica.[151] TLR9 deficiency is manifested as reduced survival, exaggerated cytokine responses, and salmonella hepatitis, while TLR2 deficiency produces the opposite effects. Deficiency of either TLR may disrupt NK cell cytotoxicity, and IFN-y and ROS production.[151]"

"Synergism is very common in TLRs. When monocyte-derived DCs have been triggered with a TLR8 ligand, TLR3 or TLR4 are also activated, resulting in expression of IL-6, IL-10, IL-12, and TNF-a elevation. These results were also confirmed by increased binding of IRF and signal transducers and activators of transcription (STAT) transcription factors to their respective DNA binding sites, which was abolished when NF-kB, p38, and phosphoinositide 3-kinase (PI3K) inhibitors were used.152 These data suggest that co-operation among TLRs is perpetuated, not only at the top level but also among different signaling pathways to ensure proper and balanced expressions of target genes."

"Synergy and tolerance of TLRs are long-established and are critical to the innate immune response. The coadministration of LPS (TLR4 agonist) and MALP-2 (TLR2 agonist) to mouse macrophages resulted in increased TNF-Diokine production.[153] Repeated treatment with LPS or MALP-2 resulted in a hyporesponse, also termed tolerance. Intriguingly, pretreatment with any ligand results in lower responses on exposure to the second ligand.[153] LPS may cause downregulation of the cell surface expression of TLR4 after the second LPS treatment; however, MALP-2- mediated reduction in responses involve modulation of downstream signaling. The acute immune tolerance and cross-tolerance between TLR4 and TLR9 have been studied,[154] indicating that LPS selectively inhibits proinflammatory cytokines, while CpG suppresses both pro- and anti-inflammatory responses. IRAK-M is critical for the induction of this differential response, and its expression is modulated by IL-7.[154]"

"Drug development is a lengthy process that starts with lead molecule identification and progresses through optimization, animal modeling studies, pharmacokinetic and pharmacodynamic studies, and preclinical and clinical stage trials. Therefore, if a drug fails to show any effect or shows toxicity in clinical studies, there must have been a series of oversights during earlier experimental stages. It is hard to give a single reason for any failure and failures may encompass complex issues, such as the use of subjective, composite, or surrogate endpoints.[165] Moreover, biases in outcome reporting and publications; underreporting of adverse events; failure to select an appropriate patient group; preference for relative outcomes, rather than absolute values; no defined core outcome sets; lack of transparency and basic science; inappropriate study population size; and lack of data integrity are among the reasons for trial failures. Finally, during clinical trials involving humans, factors that influence the drug metabolism, distribution, and secretion are diverse that predispose the pharmacokinetically and pharmacodynamically optimized drug molecules to failure."

"Researchers are expending extensive efforts to generate appropriate solutions for various inflammatory, autoimmune, and malignant conditions; however, the process is not straightforward, rather it is littered with unexpected events and outcomes, along with unknown obstructions that severely undermine the efforts of the research community."

"TLRs are among the ideal targets for exploitation in immunotherapy; however, their biology still needs to be better understood in the context of target diseases. These receptors are capable of inhibiting disease pathophysiology, as well as exacerbating inflammatory diseases. Given this dual role, it is imperative to fine tune their activation using a multidrug approach. Cumulative evidence suggests the participation of TLRs in almost all diseases is unique and can be exploited by including their ligands as adjuvant treatment during regular immunotherapy or as part of other therapeutic regimens."​

- Targeting toll-like receptor 4 signalling pathways: can therapeutics pay the toll for hypertension?

"The activation of TLRs by DAMPs plays an inherently protective role, alerting cells to damage for its resolution and repair. However, excessive or prolonged DAMP-mediated stimulation of these innate immune system receptors provokes a chronic inflammatory state that contributes to the maintenance of hypertension (McCarthy et al., 2014). Through intracellular adaptor protein-dependent signal cascades, DAMP-induced TLR activation increases the expression of pro-inflammatory genes (Akira and Takeda, 2004). TLR4 is unique in this sense, being the only TLR known to recruit four adaptor molecules and signal through two distinct pathways to produce pro-inflammatory cytokines and chemokines (Kawai and Akira, 2010). Of particular interest, a variety of cell types that have long-been associated with cardiovascular diseases have been found to express TLR4, such as macrophages, renal epithelial cells, cardiomyocytes, vascular smooth muscle cells (VSMCs), endothelial cells (ECs), glial cells and neurons (Vaure and Liu, 2014). Indeed, a myriad of studies show that abnormal activation of TLR4, primarily by DAMPs, contributes to cardiovascular dysfunction and remodelling, kidney disease and CNS dysregulation. These studies form the basis of the suggestion that DAMP-induced TLR4 stimulation may be the missing link between inflammation and hypertension."

"Table 1 contains a summary of hypertension-related DAMPs that are proposed to modulate TLR4."

"While the influence of TLR4 on BP control is not completely elucidated, TLR4 up-regulation is suggested to contribute to the pathogenesis of hypertension in animal models."

"Aldosterone, the primary human mineralocorticoid, is significantly involved in cardiovascular morbidity and hypertension (Freel and Connell, 2004)."

"[..]increased natriuresis, with a rightward shift in the sodium retention curve, contributes to the maintenance of a hypertensive state."

"TLR4 is expressed in renal epithelial cells, and its overactivation is implicated in the nephropathy associated with various diseases (Zhang et al., 2008; Souza et al., 2015). In the context of the hypertensive kidney, current literature points to AngII as the main mediator of TLR4 activation. In corroboration with this statement, it has been reported that myeloid differentiation factor 2 (MD2)-deficient mice were protected from renal inflammatory injury and fibrosis (Xu et al., 2017). The adaptor protein MD2 is known to play a role in LPS recognition by promoting TLR4–LPS–MD2 complex dimerization (Park et al., 2009). More specifically, Han et al. (2017) have demonstrated that direct hydrogen bond interactions may occur between MD2 and AngII in a manner similar to that of the MD2 and LPS interaction. Based on this evidence, it is reasonable to speculate that AngII could mediate the activation of TLR4 within the kidneys, thereby contributing to inflammation and oxidative stress, both intrinsic factors for the development of end-organ damage in hypertensive patients."

"TLR4-mediated renal damage in hypertension plays a key role in the development and progression of microvascular complications and may represent a new treatment target. Diuretics are one of the main antihypertensive drug classes targeting the kidneys, favouring water and sodium excretion to help relieve tubular pressure and lower BP. However, as AngII is produced systemically, it may continue to activate TLR4 in the face of diuretic therapy, thereby propagating renal microvascular damage. Supporting this notion, combining diuretics with angiotensin converting enzyme (ACE) inhibitors appears to produce better outcomes in hypertensive patients (Ruoff, 1989). A plausible explanation is that inhibiting AngII production may decrease the extent of TLR4 activation, ameliorating renal oxidative stress and inflammation."

"Another cause of renal damage in hypertension comes from the high BP itself, which injures the endothelial layer and contributes to elevated ROS generation. While the precise molecular mechanisms underlying the damage-induced ROS generation are not completely elucidated, recent findings showing an association between increased renal TLR4 activation and worsened outcomes in hypertensive model point to DAMP-mediated TLR4 activation (Pushpakumar et al., 2017). In the kidneys, increased levels of ROS are associated with dysfunctional glomerular and tubular cells (Araujo and Wilcox, 2014). Importantly, as NF-kB is mediated downstream of TLR4 activation and is described as a source of pro-inflammatory cytokines, this may be one mechanism by which TLR4 contributes to renal dysfunction and end-organ damage in hypertension."

"Chronic high BP and shear stress damage the vascular endothelium over time and contribute to the migration and accumulation of both innate and adaptive immune cells in blood vessels (Goulopoulou et al., 2016)."

"The promotion of inflammation is, first and foremost, a beneficial process, protecting against invading pathogens and responding to stress or injury. It is when this initial protective process becomes excessive or chronic that innate immune activation and, specifically, TLR4 signalling, can be calamitous. With overactivation, the disrupted immune homeostasis becomes pathogenic, manifesting as chronic inflammation, such as that observed in hypertension."

"In Figure 2, we present several therapeutic targets known to modulate TLR4 signal transduction, as well as potential targets for future pharmaceutical development. As illustrated, activation of TLR4 triggers two signalling cascades, which ultimately lead to the production of pro-inflammatory cytokines. Based on studies to date, it can be argued that NF-kB is implicated as the principal downstream component, orchestrating aberrant innate immune system activity in hypertension through TLR4. With similar recent findings of NF-kB dysregulation in other inflammation-associated diseases, pharmaceutical constraint of this transcription factor undoubtedly demands further exploration, particularly as a point of target given the multitude of crosstalk within the TLR4 signalling web."

"While not within the scope of this review, it is of note that all TLRs have been shown to induce NF-kB activity upon stimulation, despite their extensive diversity (Singh et al., 2014). Thus, high specificity in an NF-kB governing agent is essential to combatting potential activation of this pro-inflammatory transcription factor either by other TLR pathways or by as of yet undetermined TLR4 mechanisms. On the one hand, our lack of knowledge regarding the extent of TLR4's pathways in hypertension may result in unforeseen complications with putative therapeutics. On the other hand, the potential of supplementary connections could allow for fewer pharmaceutical risks – by targeting the component essential to disease propagation rather than the entire cascade, it is possible that the beneficial effects of TLR4 stimulation will be retained."

"Lastly, it is of critical importance that the potential risks of targeting TLR4 in hypertension be considered. As evidenced by its vast array of ligands, the TLR4 pathway plays a substantial role in shaping the immune response, and the consequences of inhibiting this arm of the immune system are still unclear."

"[..]the potential benefits of targeting TLR4 must be weighed against the risks and disadvantages of immunosuppressant treatment."​

Thanks Amazoniac! A lot to process, and all helpful.

I'm drawn to focus on understanding why my serum albumin stays low, as I imagine that if I can increase it from say 42 to 47 (and even 50), I would be able to increase my blood volume (due to albumin attracting sodium around it, and sodium increasing osmalarity and attracting more water from the ecf to plasma) and with that my blood pressure would normalize. I see the continual presence of LPS as causing albumin to be used up as quickly as it's being made by the liver. If I could find a way to deal with LPS by deactivating it and excreting it without using up albumin in the process, my serum albumin could go up. I could also increase liver albumin production and this could help too. Perhaps eating more protein would help, especially egg white.
 

Amazoniac

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Guru, you was probably bothered that those are in the gut, but since you want options that aren't pharmaceutical, you'll be narrowing your search too much if your filter removes those two; most interventions that aren't pharmaceutical will be targeting it. There can be something practical for your situation in them; for the example, circulating polyphenols after ingestion or their transdermal delivery, liposomal lactoferrin through the skin, etc. It seems that focusing on boosting the operation of internal mechanisms that deal with toxins is going to be more productive than the external aids.

- Lipopolysaccharide Is Cleared from the Circulation by Hepatocytes via the Low Density Lipoprotein Receptor

- The Systemic Inflammatory Response Syndrome (SIRS), Sepsis, and Septic Shock from 'Principles and Practice of Pediatric Infectious Diseases' (not calling you a child)
- Disorders of the Gastrointestinal System (!) from 'Equine Internal Medicine' (again, you're a robust fish, not a horse; trotting is for losers)

In case it's an active infection, more care is needed in suppressing signaling, however the body must have recognized the specifics of what it's dealing with after chronic exposure. The elevation in temperature has to be mild to not risk doing more harm than good since it's not a threatening-life matter.

All in all, these terms (antiendotoxin therapy, lps scavengers, and so on) can give you more ideas.
 
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Whichway?

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Any naturopath would tell you if you have any kind of toxic load, to first get all the bodies drainage channels (liver, kidneys, sweating, bowels) working really well, and then go low and slow on the supplements which draw out the toxins. Too much too quick will just overload your system and cause terrible Herxheimer (toxicity) reactions.
 
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yerrag

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@Amazoniac thanks for the links. From all you've shared, which I've all read, I think I have a strategy already for dealing with endotoxins in my vascular system. I would be excluding supplements and therapy directed towards reducing endotoxin on the gut level, as my problem didn't originate from the gut, but from my periodontal infection. While the periodontal infection is gone, the bacteria, and more importantly, the endotoxins, reside in the plaque in my vascular system. I don't know how extensive the pathogens and toxins are embedded in the plaque, but I'm hoping that they're mostly in the capillaries and not in the arteries, as this would be much easier to deal with. But given that they have a headstart of 15+ years, the amount of bacteria and endotoxins in my system isn't to be taken for granted.

If I were the doctor, I'm telling my patients I'm not guaranteeing success , but I'll be exhausting all efforts, leaving no stone unturned.

Simply put, my high blood pressure is merely a manifestation of low serum albumin. Low albumin is the result of high endotoxins. Albumin is used up in both binding endotoxins for eventual fecal excretion, as well as an antioxidant to deal with the oxidative stress of inflammation caused by endotoxins. The capillary plaque, aside from being a source of bacteria and endotoxins, also narrows the passage for blood flow and this contributes to higher blood pressure.

To solve my problem, I need a multi-pronged approach:

1. Continue to lyse plaque, but slowly such that the release of bacteria and endotoxins is manageable and doesn't overwhelm my immune system, such that inflammation from immunological activity is minimized. I find that the proteolytic blend of Dr. Wong's ZymEssence to be appropriate for this need, and the sole of Serraptidase to be too strong. I'm also glad to know that systemic enzymes also have some antibiotic properties that would reduce my need for antibacterials, if not totally eliminate its use.

2. Support my body so that endotoxin can be deactivated and efficiently excreted. For the endotoxin that cannot be deactivated, the support would be in terms of blunting the inflammatory effects. This would conserve the body's albumin stores, such that my serum albumin would increase to a point where it allows more sodium in plasma, thus providing for high blood volume. With higher blood volume, blood pressure would naturally lower. With less endotoxin, less albumin would be used up. With less inflammation, less albumin would be used up towards antioxidant activity.

Towards this end, the following additional supplements are what I'm considering (I have to whittle it down as it may be overkill)-

1. To deactivate LPS - progesterone, DHEA, deFibron, coconut oil (lauric acid increases cholesterol production), cocoa butter (to increase chylomicrons and triglycerides), zinc (to support alkaline phosphatase), possibly boron and copper aspirinate (not sure; it works for athritis, may work here as well)
2. To blunt the inflammatory effects of endotoxin (thru binding with LBP, then CD14, then TLR4) - vitamin A, vitamin D, B2, B3, emodin, cyproheptadine, black cumin seed oil
3. Increase blood volume - increased salt intake
4. Anti-oxidant (to conserve albumin's use as anti-oxidant) - Vitamin C, vitamin E, Glycine (needed to produce glutathione, I think)
5. Decalcification - magnesium, b6, vitamin K2
6. Anti-bacterial - essential oil nightly diffusion (the lung intake eventually leads to the blood) - cinnamon bark, eucalyptus, tea tree, or some suitable blends; colloidal silver
7. Removal of oxidized ldl or cholesterol esters in plaque - use of a cyclodextrin-based topical blend with vitamin E

This would be a good start to go with.

@Wichway you are right on those points! I had a Jarich-Herxheimer Reaction with the LPS being released into my blood at such a high rate. It was a good thing I took a CBC test and it alerted me to it through the high wbc and neutrophil count suddenly jumping up. Otherwise, I wouldn't have known what would hit me.
 
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yerrag

yerrag

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Have you tried going to a pristine location ? Or metal chelation or both ?
Not possible/oracticalto go to pristine location. But tried metal chelation for 5 years and that didn't work. In retrospect, I would have discounted heavy metal toxicity as a cause since high serum creatinine and microalbuminuria points more to a problem with the glomerular capillaries. Heavy metal toxicity would involve more the tubules.
 
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yerrag

yerrag

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For blood volume why not try either a saline iv (two liters) or saline enemas if you can't do that
That won't work. I tried increasing salt intake to no avail. I then realize that without increasing my serum albumin, I wouldn't be able to hold more salt in my blood, and without increasing salt in my plasma, water from the ecf won't be attracted towards increasing plasma volume. My albumin levels isn't increasing because it's used up in binding to endotoxins. It's also being used up as an antioxidant in countering the oxidative stresses stemming from bacteria and endotoxins.
Don't cholestyramine enemas bind endotoxin
How does that work? Haven't encountered it.

I'm also thinking about using d-mannose to flush out bacteria (thru urine) as that could be a better way to killing bacteria as killing bacteria still leaves me to deal with the endotoxins it leaves off.
 

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