Great. Even if you aren't sure of the si,e of the liposome it should still be better than nothing. Could you point me to the brand? Some brands add oil and call it liposomal even though it's not truly a liposomal formulation.
I am glad you got the liposomal form. Do you know its scale?
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The most bioavailable form of lysine is L-lysine hydrochloride (L-lysine HCl). This is the salt form of lysine, The absolute bioavailability of L-lysine hydrochloride (L-lysine HCl) likely around 50-60%
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Liposomal forms of nutrients, including lysine, are designed to improve bioavailability by encapsulating the active compound (in this case, lysine) within lipid bilayers. This liposomal delivery system protects lysine from degradation in the gastrointestinal tract and enhances its absorption through the gut lining.
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Size Matters the size of the liposomes plays a crucial role in determining their absorption efficiency. Research indicates that liposomes right around 100 nanometers (nm) tend to have the best absorption profiles.
It’s perplexing to me that atheist materialists still hold their position, given the overwhelming evidence pointing to the existence of more than just matter in motion.
Consider this simple thought experiment: if the universe – including space, time, matter, and energy – ceased to exist, would the universe itself still exist? The clear answer is "no." Yet, even in this hypothetical absence of the universe, fundamental principles of logic, such as the law of non-contradiction, would still hold true. This suggests that logic is not merely a property of the universe but something that transcends it. If the universe operates according to logical principles that exist beyond it, then it stands to reason that something beyond the material realm governs these truths, pointing to a reality deeper than physical matter alone.
Quercetin and curcumin have complementary rather than directly competitive. You are correct in that both are polyphenolic compounds with strong antioxidant and anti-inflammatory properties, but they target different molecular pathways, allowing for potential synergistic effects.
- Quercetin: Acts primarily through inhibition of pathways like NF-κB, PI3K/Akt, and JAK/STAT, and modulates various enzymes like COX and LOX, contributing to anti-inflammatory and anti-cancer properties.
- Curcumin: Primarily targets NF-κB, STAT3, and MAPK pathways and also inhibits various kinases and transcription factors.
While both affect NF-κB signaling, their precise binding sites and interactions with cellular components differ, so they do not directly compete but may enhance each other's effects, particularly in cancer research where their combination is studied for enhanced anti-angiogenesis and apoptosis-inducing activities.
Below is a more comprehensive breakdown of the Pharmacodynamic Properties of Quercetin and Curcumin
Quercetin Pharmacodynamics
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Antioxidant Activity:
- Quercetin is a potent scavenger of free radicals, reducing oxidative stress by neutralizing reactive oxygen species (ROS). It also upregulates endogenous antioxidant enzymes like superoxide dismutase (SOD), catalase, and glutathione peroxidase.
- Mechanism: Direct scavenging of radicals and inhibition of xanthine oxidase, which produces superoxide radicals.
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Anti-inflammatory Activity:
- Quercetin inhibits pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) by blocking the NF-κB pathway. It also downregulates enzymes like COX-2 and 5-LOX, reducing prostaglandins and leukotrienes.
- Mechanism: Suppression of NF-κB activation and inhibition of MAPKs (mitogen-activated protein kinases), leading to reduced expression of inflammatory genes.
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Anti-cancer Effects:
- Quercetin induces apoptosis and inhibits proliferation in cancer cells. It works by modulating the PI3K/Akt/mTOR and JAK/STAT pathways, both involved in cell growth and survival.
- Mechanism: Activation of pro-apoptotic proteins (Bax, caspases) and inhibition of anti-apoptotic proteins (Bcl-2). It also disrupts the cell cycle by regulating cyclins and CDKs (cyclin-dependent kinases).
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Angiogenesis Inhibition:
- Quercetin inhibits angiogenesis, the formation of new blood vessels, a crucial process in tumor growth.
- Mechanism: Downregulation of VEGF (vascular endothelial growth factor) and suppression of HIF-1α (hypoxia-inducible factor 1-alpha), limiting the blood supply to tumors.
Curcumin Pharmacodynamics
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Antioxidant Activity:
- Curcumin is also a strong antioxidant, directly scavenging ROS and upregulating antioxidant enzymes like glutathione. Curcumin’s antioxidant effects are closely linked to its anti-inflammatory and anti-cancer properties.
- Mechanism: Direct scavenging and upregulation of Nrf2 (nuclear factor erythroid 2-related factor 2), a transcription factor that controls the expression of antioxidant proteins.
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Anti-inflammatory Activity:
- Curcumin inhibits inflammatory mediators like TNF-α, IL-6, and IL-1β, primarily through the NF-κB pathway but also via STAT3 inhibition. It reduces the expression of COX-2 and LOX, much like quercetin.
- Mechanism: Suppression of NF-κB and STAT3, which reduces the transcription of inflammatory genes.
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Anti-cancer Effects:
- Curcumin exerts its anti-cancer effects through multiple pathways, including apoptosis induction, inhibition of cell proliferation, and suppression of metastasis. It targets the PI3K/Akt and mTOR pathways, similar to quercetin, but also impacts Wnt/β-catenin signaling, making it effective in various cancer types.
- Mechanism: Curcumin inhibits cyclin D1, CDKs, and promotes pro-apoptotic factors like p53 and caspases. It also inhibits metastasis by downregulating matrix metalloproteinases (MMPs) and modulating epithelial-to-mesenchymal transition (EMT).
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Angiogenesis Inhibition:
- Curcumin blocks angiogenesis, particularly in the context of tumor growth. It does this by inhibiting VEGF, FGF (fibroblast growth factor), and PDGF (platelet-derived growth factor).
- Mechanism: Curcumin reduces HIF-1α and VEGF expression, similar to quercetin, but also inhibits other pro-angiogenic factors like MMP-9 and angiopoietins.
Potential Synergy in Pharmacodynamics
Although both compounds have overlapping actions (e.g., inhibiting NF-κB, VEGF, and inducing apoptosis), they do not directly compete in their mechanisms. Instead, they complement each other by targeting different aspects of similar pathways or working on parallel pathways that converge at key points:
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Complementary Antioxidant Effects:
- Both quercetin and curcumin reduce oxidative stress but through slightly different mechanisms. Quercetin’s direct scavenging and enzyme inhibition (e.g., xanthine oxidase) combined with curcumin’s activation of the Nrf2 pathway provide a broader antioxidant defense.
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Enhanced Anti-inflammatory Action:
- Quercetin’s inhibition of PI3K/Akt and JAK/STAT complements curcumin’s STAT3 suppression and NF-κB inhibition, resulting in a stronger reduction of inflammatory mediators like TNF-α and IL-6.
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Dual Targeting of Apoptosis and Cell Proliferation:
- Quercetin primarily acts through Bax/Bcl-2 modulation, while curcumin also engages p53 and cyclin pathways. This allows for enhanced apoptosis and inhibition of cancer cell proliferation from multiple angles.
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Stronger Angiogenesis Inhibition:
- Both quercetin and curcumin inhibit VEGF and HIF-1α, but curcumin also suppresses FGF and PDGF, which are critical in cancer-induced angiogenesis. Together, they provide a more comprehensive blockade of blood vessel formation in tumors.
Pathways of Interest in Cancer Research
- NF-κB: Both quercetin and curcumin inhibit NF-κB, leading to reduced inflammation, decreased cancer cell proliferation, and inhibition of survival signals.
- PI3K/Akt/mTOR: Quercetin and curcumin both target this pathway, which is crucial for cell growth and survival, particularly in cancer cells.
- JAK/STAT: Quercetin's effects on JAK/STAT could complement curcumin’s suppression of STAT3, enhancing their combined anti-inflammatory and anti-cancer effects.
- VEGF/HIF-1α: Their combined suppression of VEGF and HIF-1α, critical regulators of angiogenesis, is particularly important for limiting tumor growth.
Sources:
Here is some further reading for those interested. Feel free to ask questions.
Mechanism of Action:
1. Inhibition of Lipoprotein(a) Binding
- Lipoprotein(a) [Lp(a)] and Atherosclerosis: Lp(a) is structurally similar to low-density lipoprotein (LDL) but contains an additional protein called apolipoprotein(a), which has a high affinity for damaged arterial walls. It accumulates at sites of endothelial injury, contributing to the development of atherosclerotic plaques.
- Lysine's Role: Lysine competes with Lp(a) for binding to lysine-binding sites present on the arterial wall. By occupying these binding sites, lysine prevents Lp(a) from adhering to the vascular endothelium, reducing the formation and progression of calcified plaques.
- Collagen Stabilization: Lp(a) also binds to fibrin and damaged collagen within atherosclerotic lesions, further promoting calcification. Lysine, by blocking Lp(a) and stabilizing collagen structures, helps prevent further deposition of lipoproteins and calcium.
2. Solubilization of Lipoprotein(a)
- Lysine’s Chelating Action: Lysine, along with other amino acids like proline, can enhance the solubility of Lp(a) already bound to arterial walls, helping to mobilize and dissolve existing calcified plaques. This occurs because lysine disrupts the electrostatic interactions between Lp(a) and the arterial matrix, allowing the plaque to be metabolized and cleared from the bloodstream.
- Calcium Dissolution: Lysine’s chelating properties may also contribute to the dissolution of calcium phosphate deposits in the arterial wall. Though this mechanism is less well-characterized, it is postulated that lysine interacts with calcium ions and prevents their crystallization, thereby reducing calcification.
3. Reduction of Inflammation and Oxidative Stress
- Inflammation in Atherosclerosis: Inflammatory processes within the vasculature attract immune cells that produce reactive oxygen species (ROS) and cytokines, which promote calcification by damaging vascular smooth muscle cells (VSMCs) and endothelial cells.
- Lysine's Anti-inflammatory Role: Lysine has shown some capacity to modulate inflammatory responses. By reducing oxidative stress and inflammatory mediators, lysine may indirectly prevent the calcification process, as oxidative stress accelerates VSMC calcification.
4. Interaction with Matrix Gla Protein (MGP)
- MGP and Calcification: MGP is an important inhibitor of vascular calcification. Its function is dependent on vitamin K, but some evidence suggests that lysine can also influence MGP activity, helping to prevent calcification.
- Lysine and Calcium Metabolism: Lysine may enhance calcium metabolism by interacting with calcium-binding proteins or promoting the activity of inhibitors like MGP, thereby reducing calcification by limiting the deposition of calcium salts in arterial tissue.
5. Enhancement of Collagen Production and Vascular Repair
- Collagen Synthesis: Lysine is critical for collagen production, a major structural component of the extracellular matrix in arteries. By supporting collagen formation, lysine helps maintain the integrity of the arterial wall, which may be important in preventing the mechanical damage that triggers Lp(a) and calcium deposition.
- Vascular Repair: Enhanced collagen production promotes the repair of damaged arterial walls, reducing the binding sites for Lp(a) and preventing subsequent calcification.
6. Synergistic Role with Vitamin C
- Vitamin C and Collagen Stabilization: Lysine often works in tandem with vitamin C to promote collagen synthesis and stabilize vascular walls. Vitamin C is essential for hydroxylation of proline and lysine residues in collagen, which strengthens the arterial matrix. This reduces the availability of exposed collagen and fibrin, both of which can serve as substrates for Lp(a) and calcified plaques.
- Antioxidant Synergy: Lysine and vitamin C may synergistically reduce oxidative stress, further limiting vascular calcification and plaque progression.
*** Mechanical Rational for Timing***
1. Avoiding Protein with Lysine:
- Competition with Other Amino Acids: Lysine, like other amino acids, is absorbed in the small intestine via specific transporters. If lysine is consumed along with large amounts of protein, the presence of other amino acids may compete for the same transporters, potentially reducing the absorption efficiency of lysine. This could limit the amount of lysine available for its proposed beneficial effects on vascular health, such as preventing Lp(a) binding and supporting collagen synthesis.
- Metabolic Load: High protein intake increases the metabolic load on the liver and kidneys due to the need to metabolize and excrete excess nitrogen (in the form of urea). This could divert metabolic resources from the synthesis and repair processes that lysine is involved in, such as collagen production and endothelial repair. For those focused on optimizing lysine’s vascular benefits, it may be more effective to take lysine separately, especially if the goal is to avoid competition or interference from other amino acids.
2. Avoiding Carbohydrates with Vitamin C:
- Glucose-Vitamin C Competition: Glucose and vitamin C share similar transport pathways, particularly the GLUT1 and GLUT3 transporters, which are responsible for transporting both substances into cells. High blood sugar levels or excessive carbohydrate intake can reduce the efficiency of vitamin C uptake by endothelial cells, as glucose competes with vitamin C for transport into the cells. This competition can result in reduced intracellular concentrations of vitamin C, impairing its antioxidant and endothelial-protective functions, such as nitric oxide bioavailability and collagen synthesis.
- Glycation and Oxidative Stress: High carbohydrate intake, especially refined sugars, can lead to the formation of advanced glycation end-products (AGEs). AGEs are harmful compounds that form when proteins or fats combine with sugars in the bloodstream. AGEs promote oxidative stress, inflammation, and endothelial dysfunction. Vitamin C, which is critical for reducing oxidative stress and preventing endothelial damage, may be less effective if consumed alongside high levels of carbohydrates that increase glycation processes.
- Hyperglycemia-Induced Endothelial Dysfunction: High carbohydrate intake, particularly in individuals with insulin resistance or poor glucose control, can lead to postprandial (after-meal) hyperglycemia, which is known to cause endothelial dysfunction. Vitamin C's ability to protect endothelial cells from damage could be compromised when paired with excessive carbohydrates, as the oxidative stress and inflammation from hyperglycemia may outweigh the protective effects of vitamin C.
HOPE THAT HELPS
Great read and great information from a fellow researcher!! The pharmacokinetic and pharmacodynamic profiles of both lysine and vitamin C exhibit high bioavailability under typical conditions. While liposomal formulations offer an enhancement in bioavailability, such modifications are generally unnecessary given the sufficient absorption rates of these compounds. But if you can afford it, go for it. You stated that the brand doesn't matter but it does. Some places can mix up to 40% with other compounds. So if the brand you stated worked for you, keep it! I typically call the manufacturer and have them send over their lab data, clinical data, etc.
If you're taking fenbendazole and ivermectin together, it's important to monitor for any signs of liver toxicity, such as fatigue, jaundice, or dark urine, as both medications are metabolized by the liver. Stay hydrated by drinking plenty of water, which can help support your liver and overall health.
You get it. Try thinking out of our collective lense and steelman the other side. They believe that climate change is real. So, being able to flip the idea around would turn the point invalid.
Point from our perspective: You believe humans can change the climate, so they can change the weather.
flipped point from them: You believe humans can change the weather so they can change the climate.
Essentially, rending the point invalid.