Reformulation of EGCG and Chrysin for Enhanced Lymphatic Delivery
Work has been conducted with Tom Lahey of Lutimax Nutraceuticals to reformulate EGCG, chrysin, and other natural compounds to ensure effective lymphatic system delivery without taste. This reformulation required considerable effort and has resulted in improved formulations.
Discontinuation of Previous EGCG Preparation
YUCKKO is discontinued. The EGCG-coconut milk mixture is optional and can be continued at the individual’s discretion.
Core Protocol Adjustments: New Formulations Introduced
The original HIV treatment protocol remains unchanged except for the inclusion of EGCGSyn and ChrySyn.
Importance and Synergism of Chrysin and EGCG
Chrysin, found in honey and other natural sources, demonstrates significant synergistic effects with EGCG. However, due to its low water solubility and limited bioavailability, most online chrysin products are ineffective. Although coconut milk may increase its bioavailability, the ChrySyn formulation—developed using patented methods—offers superior efficacy.
EGCGSyn and ChrySyn, formulated with FDA-approved emoluments that enhance lymphatic targeting, are notable for their stability and biological activity. The emoluments used are scientifically validated by their manufacturers.
Stabilization of Polyphenols
EGCG, which contains eight hydroxyl groups prone to rapid oxidation, has been stabilized in the new formulation to extend its bioactivity. Oxidation typically inactivates flavonoids and polyphenols, reducing therapeutic effectiveness.
HIV Pathogenesis and Mechanisms of Action
Initial success with EGCG in early HIV infections may be attributed to its activity against CCR5 macrophage-tropic viruses. EGCG shows limited or no activity against CXCR4 CD4 T cell-tropic viruses in established infections. EGCG is effective in slowing or halting macrophage infections but does not affect T cell infections.
Mechanistic Insights: ChrySyn and EGCGSyn Synergistic Potential
It is proposed that EGCGSyn and ChrySyn together can fully suppress HIV synthesis. The HIV Rev protein activates casein kinase II (CK2), phosphorylating key viral proteins. Chrysin acts as a CK2 inhibitor and is more effective than quercetin.
Inhibition of HIV Transcription Factors
To suppress HIV synthesis effectively, two transcription factors must be neutralized: NF-kappaB and c/ebp beta. EGCG functions as a proteasome inhibitor comparable to FDA-approved Velcade, thereby blocking NF-kappaB. However, EGCG does not inhibit c/ebp beta.
Blocking only NF-kappaB is insufficient to achieve low viral titers; c/ebp beta must also be inhibited.
Role of Prostaglandins in HIV Activation
PGE2 stimulates HIV synthesis in T cells by activating c/ebp beta. Thus, prostaglandin inhibitors like ibuprofen are no longer recommended.
NF-kappaB and c/ebp Beta Synergy in HIV Activation
Chrysin’s ability to downregulate COX-2 synthesis is linked to inhibiting NF-IL6 (also known as c/ebp beta) binding to DNA.
Biochemical Effects of Chrysin and EGCG
Chrysin:
- Inhibits c/ebp beta DNA binding
- Inhibits CK2 enzyme activity
EGCG:
- Blocks HIV binding to CD4
- Inhibits the proteasome and PI-3k activity
- Inhibits stat1 activity in macrophages
NEF-mediated HIV synthesis in macrophages involves stat1 activation.
Additional Compounds and Administration Tips
Quercetin may be used to support EGCG and chrysin activity. It also occupies hepatic degradation enzymes, prolonging the half-life of EGCGSyn and ChrySyn.
NAC, ALA, vitamin E, and other antioxidants remain part of the protocol. NAC’s low bioavailability may be improved by mixing with coconut or buttermilk. ALA should be taken in buttermilk to avoid curdling.
Dosage Guidelines
EGCGSyn:
- 3 grams/day (rounded teaspoon)
ChrySyn:
- 1 gram/day (flat teaspoon)
Take on an empty stomach once daily. Doses can be doubled based on individual HIV infection status. These compounds are non-toxic.
Replacement of Prior EGCG Preparation
EGCGSyn replaces the 70% EGCG preparation previously mixed with coconut milk. While continuing to use coconut milk-formulated EGCG is optional, ChrySyn is considered essential due to its unique bioavailability.
Foundational Principles of the HIV Treatment Protocol
Natural Medicines as Viable Alternatives to Antiretroviral Therapy
Evidence suggests that HIV/AIDS may be managed using natural medicines and over-the-counter supplements. Validation of these approaches depends on the replication of outcomes, particularly in resource-limited regions.
Mechanism of Action of Conventional HIV Medications
Antiretroviral therapies (e.g., AZT and protease inhibitors) target:
- Reverse transcriptase (RT) to prevent viral DNA integration
- HIV protease to block the formation of infectious virions
However, non-infectious HIV particles also exert harmful effects.
Misconceptions About Protease Inhibitors
While protease inhibitors lower viral RNA in the blood, this effect is not attributable to direct inhibition of HIV protease. These drugs likely inhibit synthesis via suppression of CK2 and the proteasome.
CK2: A Central Activator in HIV Pathogenesis
CK2 phosphorylates multiple HIV proteins, including:
- RT
- REV
- VPU
- Protease
Protease inhibitors likely function by inhibiting CK2 rather than HIV protease directly.
Role of Natural Compounds in HIV Suppression
Natural compounds with inhibitory effects:
- Quercetin → CK2 inhibitor
- EGCG → Proteasome inhibitor
These compounds mimic the biochemical effects of standard antiretrovirals.
Strategy for Protocol Development
The protocol was developed by:
- Identifying critical biochemical pathways
- Matching them with natural compounds
- Utilizing coconut milk to target the lymphatic system
Volunteer Testing and Outcomes
Three volunteers tested the protocol. Immune function improved:
- CD4 counts increased
- HIV titers decreased
- Immune restoration observed
“Adam’s Story” details one case involving dual HIV and hepatitis B infection. CD4 count: 1150. HIV titer: 5200.
Transition from Antiretrovirals to Natural Protocol
Gradual transitions from standard therapies to natural protocols are advised under medical supervision.
Scientific Community Response and Future Direction
Challenges in Gaining Acceptance
Efforts to disseminate this protocol have received limited attention from mainstream scientific institutions. Despite skepticism, the protocol has shown efficacy in case studies.
Multi-Pathway Targeting with Natural Compounds
Modern drug development focuses on specificity. In contrast, natural compounds impact multiple pathways. When compounds are strategically combined, this broad activity allows for comprehensive disease management.
HIV Treatment Protocol Summary
Accessibility and Use
In the U.S. and Canada, all the protocol supplements are available without prescription. Products can be obtained from health food stores, supermarkets, pharmacies, and online retailers.
Part One: Background on Natural Compounds in Disease Treatment
Laboratory Studies and Clinical Limitations
The scientific literature contains thousands of references to using natural products, such as plant-derived molecules, for treating a wide range of diseases. Most of these studies are conducted in laboratory settings using culture dishes. Promising results, such as plant-derived products inhibiting HIV synthesis, often do not translate into clinical success due to several limitations.
Solubility and Delivery Challenges
Many natural compounds are not soluble in water, making it difficult for them to be absorbed into the body. In laboratory settings, these compounds are dissolved in DMSO or alcohol and diluted in tissue culture media. While these methods reveal potential utility, they are not viable for human use due to the toxicity of such solvents. Therefore, either alternative delivery methods must be found, or development is halted—this marks an early fork in the road in drug development.
Transition from Laboratory Research to Clinical Application
Basic scientists identify compounds capable of inhibiting disease mechanisms, but translating these findings into viable pharmaceutical products requires addressing issues such as solubility and delivery. Clinical scientists may modify the compounds or develop novel delivery systems to circumvent the limitations of solvents like DMSO or alcohol.
Glycoside vs. Aglycoside Forms
Natural medicines such as quercetin and curcumin are glycosides (water-soluble but biologically inactive due to the sugar molecule) and glycosides (biologically active but water-insoluble). Glycosides are typically used in laboratory studies and are difficult to absorb into the body in their unmodified form. Health supplements often contain a mixture of both forms.
Absorption and first-pass Metabolism
Even if absorption occurs in the intestinal wall, compounds may be chemically modified and returned to the intestines. If they enter the portal blood system, the liver metabolizes and often destroys them before systemic distribution—a challenge known as the First Pass Phenomenon. The liver protects against harmful substances but also hampers drug delivery to target sites like tumors or HIV-infected cells.
Bioavailability Limitations of Oral Supplements
Most natural medicines in pill or capsule form have low bioavailability. Consequently, oral supplementation is unlikely to achieve therapeutic concentrations. This issue is well-known in the supplement industry but seldom communicated to consumers.
Part Two: Enhancing the Bioavailability of Natural Products
Two Main Pathways of Absorption
Molecules typically enter the body through either:
- Portal Blood System – Suitable for amino acids and carbohydrates but problematic due to liver metabolism.
- Lymphatic System – Designed for the absorption of fats and fat-soluble substances.
Mechanism of Lipid-Based Delivery via the Lymphatic System
Ingested fats are broken down into fatty acids and monoglycerides, which are absorbed into the intestines and then reassembled into triglycerides. These are transported into the lymphatic system, not the blood. Fat-soluble molecules co-dissolved in fats can also enter the lymphatic system through this pathway.
Role of the Lymphatic System in Drug Delivery and Immunity
The lymphatic system delivers oxygen and nutrients, removes waste, and serves as the site of the immune response. HIV resides in the lymphatic system rather than the blood, making it a critical target for treatment.
Use of Coconut Milk for Lymphatic Delivery
Some pharmaceutical companies employ liposomes to deliver poorly soluble drugs to the lymph. In this protocol, coconut milk was used as an accessible fat-based delivery vehicle. Coconut milk, made by emulsifying coconut water and coconut meat, contains high levels of coconut oil (a saturated fat) and enhances the bioavailability of natural products.
Properties of Coconut Oil
Lauric acid, the primary fat in coconut oil, cannot accumulate in arteries and supplies substantial energy. Lauric acid and its derivative monolaurate exhibit antiviral properties against enveloped viruses like HIV and hepatitis. SDS (sodium dodecyl sulfate), a potent detergent, is a sulfated form of lauric acid used in consumer products such as toothpaste.
Protocol for Coconut Milk Preparation
Natural compounds were dissolved in coconut milk by boiling it and cooling it to room temperature before consumption. This method enhances lymphatic absorption of compounds that are otherwise poorly bioavailable.
Part Three: Detailed HIV Treatment Protocol
Application Across All Stages of HIV Infection
The protocol can be applied at any stage of HIV infection. Adjustments for clinical AIDS (symptoms like wasting or diarrhea) are discussed separately.
Core Ingredients for Lymphatic Delivery
- Quercetin
- Dosage: 6 grams daily (3 grams AM, 3 grams PM), boiled in coconut milk.
- Mechanism: Inhibits HIV synthesis by blocking CK2 and 5-nucleotidase.
- Notes: Select products with minimal grit.
- EGCG (Epigallocatechin gallate)
- Dosage: 6 grams daily (3 grams AM, 3 grams PM), boiled in coconut milk.
- Requirement: 70% EGCG and 99% total green tea polyphenols (e.g., Green Tea-70).
- Mechanism: Inhibits HIV replication pathways and improves CD4 counts.
- Note: Avoid green tea powder or drinks due to theanine content.
- Silymarin (Milk Thistle Extract)
- Dosage: 1 gram daily (500 mg AM, 500 mg PM), added to warm coconut milk after cooling.
- Mechanism: Inhibits ETS gene activation pathway influenced by HIV protein NEF.
Additional Supplement Components
- Nicotinamide (Niacinamide)
- Dosage: 1 gram in the morning.
- Function: Replenishes NADH/NADPH and inhibits DNA activation by ADP-ribosylation.
- Melatonin
- Dosage: 20 mg at night (maximum 3 mg/day for those with clinical AIDS).
- Function: Enhances immune response and acts as an antioxidant.
- NAC (N-acetylcysteine)
- Dosage: 6 grams daily (3 grams AM, 3 grams PM).
- Function: Boosts intracellular GSH in lymphoid cells.
- ALA (Alpha Lipoic Acid)
- Dosage: 2 grams daily (1 gram AM, 1 gram before dinner).
- Function: Antioxidant, NF-kappaB inhibitor, neutralizes peroxynitrite.
- Vitamin C Esters
- Dosage: 2 grams daily in divided doses.
- Function: Enhanced antioxidant support.
- Vitamin E
- Dosage: 2000 IU daily in divided doses.
- Function: Supports immune function and cellular health.
- Sodium Selenite
- Dosage: 250 mcg daily in the morning.
- Requirement: Only sodium selenite form is effective.
- Magnesium Sulfate
- Dosage: ½ teaspoon of juice in the morning.
- Function: Essential for enzyme systems; Epsom salts recommended.
- Inosine
- Dosage: 500 mg in the morning.
- Function: GTP precursor enhances immune response in combination with quercetin.
- L-Carnitine
- Dosage: 2 grams daily (1 gram AM, 1 gram PM).
- Function: Facilitates fatty acid metabolism and prevents ceramide-induced cell death.
Part Four: Administration Guidelines
Preparation and Consumption
- Only quercetin and EGCG are boiled in coconut milk; silymarin is added after cooling.
- Use capsules, not tablets; gelatin capsules can be dissolved directly in the milk.
- Do not use microwave heating.
- Heavy cream may be used as a substitute if coconut milk is unavailable.
Absorption Considerations
- Best taken on an empty stomach to improve absorption.
- The fat content in coconut milk or heavy cream is essential for lymphatic delivery.
Protocol Adherence
- No changes or omissions should be made to the protocol for optimal effectiveness.
- Partial adherence may result in reduced therapeutic outcomes.
Part Five: Diet and Lifestyle
To maximize the effectiveness of this protocol, it is critical to avoid certain substances that can negatively impact immune function.
- Alcohol and Smoking: Both alcohol and smoking generate free radicals, which can enhance the synthesis of HIV.
- Soy Products: Avoid soy products as they contain genistein, an isoflavone that blocks lymphoid cells in the G2 phase of the cell cycle. Since the HIV virus is primarily made during the G2 phase when the HIV gene is most exposed, this prolonged G2 phase can lead to an increase in viral production. Studies have shown that substances like caffeine, which block the G2 pause in lymphoid cells, can decrease HIV synthesis by up to 92%. Theophylline, an asthma medication, has similar effects. In contrast, genistein promotes HIV production, while caffeine and theophylline inhibit it, especially in T cells.
- Caffeine: Drink caffeine-containing beverages, but avoid caffeine pills, as they release too quickly. Tea, such as orange pekoe, contains as much caffeine as coffee. It is also important to note that darker coffee roasts, like espresso, contain less caffeine due to the roasting process.
- Healthy Diet: Aim for a balanced diet while minimizing foods that contain high levels of arachidonic acid, such as butter and fatty meats. Arachidonic acid, once converted to prostaglandins and leukotrienes, can interfere with immune function. Recommended oils for cooking include canola and coconut oils, while corn, safflower, and soy oils should be avoided. Olive oil is also a good choice. Opt for lean meats like skinless chicken and turkey, and focus on oily fish, such as salmon, tuna, and sardines, which provide healthy fatty acids that support immune health.
Part Six: The Three Amigos
Three volunteers participated in testing this protocol, each experiencing different challenges. Their stories highlight the importance of perseverance in the fight against HIV.
- Adam’s Journey: Adam, initially feeling fine, was unknowingly facing a severe decline in health. As his viral load decreased and his immune system was reactivated, he experienced fever and nausea—common reactions when fighting off an infection. The HIV virus primarily resides in the intestines, making intestinal viral attacks especially uncomfortable. Over time, Adam’s health improved significantly, with fewer illnesses and substantial improvements in his allergies.
- Eric’s Experience: Eric began with a viral count of 214,000 and a CD4 count of 557. The protocol initially involved curcumin and quercetin, which proved less effective than expected. While curcumin inhibited HIV synthesis, it also hindered CD4 cell counts. Switching to EGCG resulted in a significant improvement, with Eric’s HIV count dropping to 25,000 and his CD4 count rising to 662. His condition improved with continued treatment.
- Blanche’s Remarkable Recovery: Blanche’s story was particularly noteworthy. After years of antiretroviral treatment, her HIV count was undetectable, but her CD4 count remained below 550. After losing access to her HIV medication, Blanche turned to this protocol. Within a week, her CD4 count increased by 200 points, a remarkable improvement. However, Blanche faced complications when she contracted shingles, a reactivation of latent herpes zoster. This triggered a cascade of immune responses, weakening her system. By adjusting her protocol, Blanche’s health rebounded, and her immune system began to recover.
Blanche’s experience highlights that a CD4 count below 200, traditionally considered a threshold for AIDS, does not necessarily equate to the onset of AIDS. Several factors, including stress, malnutrition, and co-infections, contribute to the progression of AIDS. In Blanche’s case, despite a low CD4 count, she did not develop AIDS. The key was managing her immune system with the right supplements despite numerous opportunistic infections.
Part Seven: What is AIDS?
In the essay The Day AIDS Ceased to be Fatal, the authors propose that clinical AIDS is essentially a form of adrenocortical insufficiency, akin to Addison’s disease. Symptoms such as diarrhea, anorexia, and wasting can be linked to a gradual decline in the body’s ability to bind the glucocorticoid hormone cortisol, often exacerbated by HIV proteins and opportunistic infections. Once cells become resistant to cortisol’s anti-inflammatory effects, a biochemical cascade occurs that mimics adrenocortical insufficiency, leading to what is recognized as clinical AIDS.
A case study further illustrates this idea. A woman with advanced AIDS, after being treated with prednisone, regained her health and left the hospital in just three days. Over the next month, she gained 20 pounds and returned to work. This rapid improvement suggests that corticosteroid treatment, when administered in appropriate doses, can reverse AIDS-related symptoms, though it does not cure the HIV infection itself.
For those with clinical AIDS, a physician-prescribed hormone replacement dose of methylprednisolone may be beneficial. This approach can restore the body’s ability to respond to cortisol and improve immune function. However, it is important to note that cortisol cannot restore the immune system by itself—it plays a crucial role in preventing AIDS. Thus, combining this approach with the recommended treatment protocol can be the most effective strategy for addressing clinical AIDS.
In the absence of clinical AIDS, hormone replacement is not required. It is critical to understand that CD4 count alone does not determine the presence of AIDS. Rather, the ability of the body’s cells to bind cortisol is the key factor in preventing AIDS.
Part Eight: Overview
- If you have an active hepatitis B infection, you should not use EGCG at first. Use the protocol with quercetin and other supplements, but leave out the EGCG. EGCG is a potent inhibitor of the proteasome complex, which may activate the hepatitis B HBX protein and induce viral synthesis. Once the active infection has gone back to latency, EGCG can be gradually reintroduced, starting at 1 gram per day and increasing until a maximum of 6 grams daily.
Scientific Background Information
This section provides an in-depth understanding of the mechanisms discussed in the protocol, beginning with the biochemical impact of certain compounds on HIV infection and immune response.
Quercetin and HIV Suppression
- Quercetin is a powerful inhibitor of CK2 (casein kinase II), an enzyme that activates NF-kappaB, which is essential for HIV replication. Additionally, EGCG blocks the effects of the viral NEF protein, the only viral protein capable of causing AIDS. This inhibition of NEF by EGCG is key in preventing HIV replication and supporting CD4 cell recovery.
The Role of NEF in HIV and AIDS
- NEF is central to HIV’s ability to cause immunosuppression. It not only activates pathways that affect the immune system but also sequesters CD4 T cells in the lymphatic system, preventing them from circulating in the blood. This results in a low CD4 count, characteristic of HIV infections.
- The presence of NEF in infected cells leads to the activation of pro-inflammatory pathways, causing a shift in immune function that favors inflammation over defense. This is critical in the development of clinical AIDS.
EGCG as a Key Component in HIV Treatment
- EGCG (Epigallocatechin gallate) plays a major role in inhibiting NEF and improving CD4 T cell count. EGCG has shown to be particularly effective in reversing the sequestration of CD4 cells, leading to a rapid increase in their numbers in the bloodstream. This process contributes significantly to the improvement in immune function observed in HIV patients treated with EGCG.
NEF and Protein Kinase C-Epsilon (PKCe)
- NEF has been shown to downregulate the expression and activity of PKCe, an enzyme essential for various immune functions. PKCe is involved in lymphocyte migration and activation, which is crucial for immune responses. By inhibiting PKCe, NEF effectively traps immune cells like CD4 T cells in lymphoid organs, preventing their proper activation and movement.
The Impact of NEF on Lymphocyte Migration
- NEF’s action on PKCe leads to the impairment of lymphocyte migration from secondary lymphoid organs into the bloodstream, which in turn causes CD4 lymphopenia (a reduction in CD4 cells in the blood). This phenomenon is a hallmark of HIV infections and contributes to the virus’s immunosuppressive nature.
Sphingosine-1-Phosphate (S1P) and Immune Suppression
- S1P is a molecule critical for lymphocyte trafficking. High concentrations of S1P in blood and lymph inhibit lymphocyte activation and proliferation. The combination of NEF and S1P leads to the sequestration of CD4 T cells within lymphoid tissues, exacerbating the immunodeficiency seen in HIV-infected individuals.
The Role of PKCe in Immune Function
- PKCe plays several roles in immune function, including activating macrophages and dendritic cells, which are vital for detecting and responding to infections. NEF’s inhibition of PKCe disrupts these immune functions, preventing an effective immune response to HIV and other infections.
NEF and the Development of Clinical AIDS
- The combination of NEF-induced dysfunction in PKCe and the activation of STAT1-dependent pathways contributes to the progression from HIV infection to clinical AIDS. As NEF inhibits immune responses and promotes inflammation, it plays a central role in the breakdown of the immune system, leading to the symptoms associated with AIDS.
STAT1 Signaling in AIDS
- STAT1, involved in the gamma interferon pathway, is another key target of NEF. Prolonged activation of STAT1 causes immune system dysfunction, including diarrhea, muscle wasting, and a shift from cell-mediated immunity toward humoral immunity. This shift weakens the body’s ability to fight off infections, which is one of the hallmark features of clinical AIDS.
Impact of EGCG on STAT1
- EGCG is noted for inhibiting STAT1 signaling, which helps prevent the immune suppression associated with prolonged gamma interferon signaling. This inhibition is crucial in counteracting the effects of NEF and p17, proteins that can contribute to the pathogenesis of AIDS.
Credited to: Stephen Martin, Ph.D
Chief Scientist, Grouppe Kurosawa
All Rights Reserved