Phosphoethanolamine & Meclizine: inhibiting an enzyme required to form the building blocks of membranes

Summary

Actually, the title (inhibiting an enzyme required to form the building blocks of membranes) refers to Meclizine since as we will shortly discuss below, Phosphoethanolamine acts (probably) on mitochondria.

The compound, Phosphoethanolamine, has been shown to kill tumor cells (A. K. Ferreira et al. Anticancer Res.32, 95€“104; 2012) at the University of S£o Paulo in Brazil. As a result some chemists at the University of Sao Paulo’s campus in Sao Carlos have manufactured the compound for years and distributed it to people with cancer for free. Some of those patients have claimed remarkable recoveries. (Ref). Here are some youtube movies that are connected to this subject: Ref
Here is the official website where clinical cases are presented and here is the main Facebook page that was used to create awareness about the phosphoethanolamine effects in humans and that includes testimonials from various patients.

Prof. Gilberto Orivaldo Chierice, now a retired university professor, was the one who was in charge of studies for over 20 years (Ref).

The Brazilian government announced at the end of October 2015 that it will set up a workgroup to study the effects of a substance called phosphoethanolamine, after it showed good results in cancer treatment: http://news.xinhuanet.com/english/2015-10/30/c_134765590.htm
At least 20 Brazilian states having demonstrations in favor of Phosphoethanolamine Synthetic on Nov 29th, 2015: Ref1 Ref2

And here is the Facebook page that should keep you up to date with the evolution on this subject: https://www.facebook.com/FosfoetanolaminaTestimonials; https://www.facebook.com/PhosphoethanolamineSynthetic/; and a related thread on Inspire: Ref

Nature news: http://www.nature.com/news/drugs-on-demand-1.18873

Phosphoethanolamine is an important building block of the lipids that make up cell membranes. The mechanism behind killing the cancer cells is not yet clear. However, it has been recently shown that if we just take this metabolite and directly add it to mitochondria, it actually inhibits the respiration (Ref) which may be connected with its anticancer effects when used in higher dose.

However there may be an even better alternative to the administration of Phosphoethanolamine. That is Meclizine, an over-the-counter antihistamine drug used for decades to treat nausea and motion sickness.

According to a relatively recent publication (Ref), Meclizine administration leads to a sharp elevation of cellular phosphoethanolamine (an intermediate in the ethanolamine branch of the Kennedy pathway of phosphatidylethanolamine biosynthesis) as a result of a direct inhibition of the cytosolic enzyme CTP:phosphoethanolamine cytidylyltransferase (PCYT2). Therefore, inhibition of PCYT2 by meclizine led to rapid accumulation of its substrate, phosphoethanolamine, which is itself an inhibitor of mitochondrial respiration. (Ref)

So the nice point about Meclizine is that

• it will inhibit an enzyme that is required to form the building blocks of membranes which is expected to be detrimental to cancer cells and even more to the fast progressing cancers
• as a result of the above it will lead to sharp elevation of cellular phosphoethanolamine which in turn will/may? lead to the anti cancer effects observed in the Brazilian studies (possibly due to the respiration inhibition)

Here is a nice discussion on Meclizine

• Reference 1 
• Reference 2

Updates Dec 8th, 2015: Note that Phosphoethanolamine has been discovered in 1941, by the US scientist Erwin Chargaff, Columbia University, and patented by the well known German alternative medicine practitioner dr. Hans Alfred Nieper (this is one of the first doctors using B17 / Laetrile / Amygdalin as an anti cancer treatment and who successfully? treated President Ronald Reagan for his colon cancer in 1985). Indeed, Nieper patented, together with Franz Kohler, Calcium 2-aminoethylphosphate (Calcium AEP), which he believed could be helpful in combating such diseases as juvenile diabetes, gastritis, ulcer, thyroiditis, Myocarditis and Hodgkin’s Disease (Ref). Ca-AEP or Ca-2AEP is the calcium salt of phosphorylethanolamin and it is manufactured by many nutraceutical companies, sold online and in health food stores (Ref1, Ref2).

Here is a little more on Ca-AEP

• http://www.health-science-spirit.com/EAP.html
• http://nutritionreview.org/2013/04/calcium-aep-membrane-integrity-factor-aids-treatment-multiple-sclerosis-asthma-osteoporosis/

And here is a group on Facebook using Ca-AEP https://www.facebook.com/groups/1757778211120919/

Therefore, Phosphoethanolamine or its anti cancer action was not discovered in recently in Brazil but way back at the middle of last century in US/Germany. What the scientist in Brazil did unique was on one hand to invent a way to produce Phosphoethanolamide very cheap and on the other hand to give that to many people for free and apparently cure some of them. To me, this is as valuable as discovering Phosphoethanolamine. To read the patent of the Brazilian scientists on the fabrication of Phosphoethanolamine you can go to the Brazilian patent office. Here is a blog of a Brazilian cancer patient explaining how to do that http://vaderetrocancer.blogspot.nl/2015/11/processo-de-fabricacao-da.html. If that is not possible, you can access the patent here Brazilian Patent on Phospho. The patent is in Portuguese but it can be translated with Google Translator.

Case Reports and Clinical Trials

Here is the official website where clinical cases are presented and here is the main Facebook page that was used to create awareness about the phosphoethanolamine effects in humans and that includes testimonials from various patients.

Mechanism

Phosphoethanolamine: Unknown but as discussed above possibly due to the respiration inhibition.
Here is a picture that indicates a different mechanism. And here is an animation on the same.
It is also claimed to be an anti angiogenesis inhibitor.

Meclizine: elevation of  Phosphoethanolamine and inhibition of an enzyme that is required to form the building blocks of membranes (Ref.)

Note: menaquinone (vitamin K2)  also kills cancer cells by elevating phosphoethanolamine http://www.ncbi.nlm.nih.gov/pubmed/26175011 “One of the most significantly affected metabolites was phosphoethanolamine, which exhibited a two-fold increase in menaquinone-treated Jurkat cells compared to vehicle-treated cells at 24 h, growing to a five-fold increase at 72 h. Phosphoethanolamine elevation was observed prior to the induction of apoptosis, and was not observed in menaquinonetreated lymphoblasts or chemotherapeutic-treated Jurkat cells.”

“One metabolite identified as significantly different in OCSCs, phosphoethanolamine, is a substrate for many cell membrane phospholipids that has recently been shown to induce both cell cycle arrest and apoptosis in cancer cells [15,16]. Here, intracellular phosphoethanolamine levels for OCSCs (and OCCs even though it is not a significant effect) stay fairly consistent over 48 hours for the control cells, but for the metabolic perturbations, the levels steadily increase over 48 hours. Because the phosphoethanolamine levels increase slightly but consistently for all metabolic perturbations, the reaction seems to be a generalized metabolic stress response. This reaction could be indicative of increased phospholipid membrane turnover or an apoptotic response to the increasing stress levels.” http://bmcsystbiol.biomedcentral.com/articles/10.1186/s12918-014-0134-y

Safety/Toxicity

Meclizine is an over-the-counter drug so its safety profile is good, primary side effect being drowsiness.

Preparation & Administration

Phosphoethanolamine:

I do not have clarity on the dose and adminitration protocol. However, I do have the following reference points:

• In Brazil it is administrated as capsules (probably 500 mg each capsule – to be clarified), 3x/day. Results have been observed after one month administration and no side effects have been observed.
• In the published articles the effective dose administrated to mice was 80mg/kg (Ref1 Ref2). To humans this translates to 80/12, i.e. about 7mg/kg/day. That is about 400mg/day.
• A patent suggesting 800mg/day (Ref.)

Based on the above, the assumption is that a starting dose of 400mg/day is safe.
Note that I was informed by Phosphoethanolamine Synthetic – The C. cure that “according to Dr. Meneguelo, one of the Phosphoethanolamine scientist , the patient has to take 3 oral capsules per day. But before taking the capsules should take one tablespoon of olive oil because the substance is fat-soluble.”

I actually believe that the olive oil is needed to enable the mechanism that is being claimed, i..e Phosphoethanolamine will interact with fatty acid in the liver to form the component required to have the anti cancer effect as indicated in this picture.

Update 05.Dec.2015: more info received suggesting first 60 capsules taken 3x/day. This will be enough for 20 days. After that, take one capsule 2x/day; each capsule has about 315 mg Phosphoethanolamine and other components (unknown) up to 500 mg. Before taking each capsules we should take one tablespoon of olive oil.

Here are some discussion on administration as well. And here is a google translation of a statement of RENATO Meneguelo: “The substance is fat-soluble , if there is the means she will not act because there dilue in water, 3 capsules a day before a tablespoon of extra virgin olive oil. The diet should be as healthy as possible if the patient achieve the best is a high calorie diet , it is necessary that the immune system is intact.” as shared by one of the members of a discussion in Brasil (Ref.)

Here is another interesting piece of info (again google translation) suggesting that 1g Phospo/ day is safe and was used in Brasil on humans:

Parkinson’s Disease and Phosphoethanolamine: The phosphoethanolamine is metabolized in phosphatidylethanolamine, major phospholipid mitochondrial membrane and a major responsible for maintaining the transmembrane potential – Deltapsi-m – the mitochondria. The phosphoethanolamine administered at 500mg twice a day, is converted in the liver in the three phospholipids constituents of the mitochondrial inner membrane: phosphatidylethanolamine, phosphatidylcholine, and phosphatidylserine. These three phospholipids are involved directly in the permeability of the inner membrane of mitochondria and directly interfere in transmembrane potential, Deltapsi-m.  The earliest event produced by mitochondrial injury is to change the transmembrane potential Deltapsi-m and only the change of this potential has already drastically decreases the production of ATP, in a continuous process whose sequence causes change of Complex I . and other components of the mitochondrial electron chain. Patients with Parkinson’s disease showed reasonable improvement of movement and posture with the use of only phosphoethanolamine (Prof.Gilberto Chierice and Dr. Bicudo Dair Piai – personal communication). (Ref)

Ca-AEP Intravenous:

As mentioned below, Ca-AEP can be ordered without prescription in intravenous form at German pharmacies. It is suggested to be given one vial/day, 2-3x/week. The days in between the intravenous administration it is suggested to take 1-3 capsules Ca-AEP 3x/day. (Ref.)

For gastritis, the content of two vials is suggested to be taken early in the morning before breakfast on empty stomach.

Meclizine: 25mg 2x/day (one capsule with breakfast and one with dinner) seems to be safe (Ref)

My Opinion: To maximize the potential of the therapy I would combine the administration of Vitamin K2 with Phosphoethanolamine and with Meclizine.

Source & Cost

Phosphoethanolamine (CAS Number 1071-23-4, Formula: C₂H₈NO₄P): Sigma (>98%), Santa (>96%), Carbosynth (>95%)
Info on the substance: http://www.drugbank.ca/drugs/DB01738
Sigma: http://www.sigmaaldrich.com/catalog/papers/24201752

Indeed, the following statement supports the fact that the drug can be bought from the chemical suppliers such as Sigma or Santa: <<The USP also said that the substance “is available on the market, produced by chemical plants, and can be purchased in large quantities by public authorities. There is therefore no justification for forcing the USP to produce it without quality assurance. The court orders will be fulfilled within the capacity of the University “, he said.>> Ref

A few more details:  According to this article https://pt.wikipedia.org/wiki/Fosfoetanolamina the product with CAS number 1071-23-4 is the same as Phosphoethanolamine used in Brasil. Also, note that Phosphoethanolamine has multiple synonyms, http://www.hmdb.ca/metabolites/hmdb00224. The formula NH2CH2CH2OPO3H2 is the same (linear) formula of the sigma product http://www.sigmaaldrich.com/catalog/product/sigma/p0503… which is the same with C2H8NO4P.

As Ca-AEP or Ca-2AEP (calcium salt of phosphorylethanolamin): Source1, Source2, Source3
However, I am not sure if these are the best sources since each capsule seems to include  about 6% 2-amino Ethanol Phosphate. This would be about 30mg 2-amino Ethanol Phosphate (out of a 500mg capsule), which is 10% of a capsule as given in Brasil and which must be taken 3x/day. In other words, to achieve the anti cancer dose use in Brasil, we would need to take 30 capsules/day … As a result, buying it from the chemical suppliers as a raw product and making capsules out of that is probably the best way.

Update 03-July-2016: I actually found out sources of Ca-AEP that may contain much higher levels of Phosphoethanolamine:

• Solaray, containing 438mg Phospho in 500mg capsules http://www.vitaminshoppe.com/p/solaray-calcium-eap-500-mg-60-capsules/so-1569#.V3jO87h942w
• wellnessresources, containing 825mg in 1g capsule http://www.wellnessresources.com/products/calcium_aep.php#ingredients_dosage

In German pharmacies, Ca AEP can even be found in Intravenous form, withouth prescription: https://www.medizinfuchs.de/CALCIUM%2BEAP%2BAmpullen.html?sac=1  under the PZN number 00167792, made by Köhler Pharma GmbH. Here is another source https://www.europa-apotheek.com/calcium-eap-ampullen-0167800.html.

Meclizine:

It is sold under the brand names Bonine, Bonamine, Antivert, Postafen, Sea Legs, and Dramamine (Less Drowsy Formulation). https://en.wikipedia.org/wiki/Meclizine

6 euro for 25 capsules:
https://www.apotheek-online.be/postafene-comp-25x25mg
http://www.pharmamarket.nl/postafene-25-mg-25-tabletten.html

Synergists & Antagonists

2DG: Since Meclizine shifts cell’s reliance from oxidative phosphorylation (OXPHOS) to glycolysis, combination with glyco inhibitors such as 2DG (see 2DG section on this website) may represent a good combination.

References:

Meclizine drug has the potential to treat certain infectious diseases and cancer http://www.news-medical.net/news/20131031/Meclizine-drug-has-the-potential-to-treat-certain-infectious-diseases-and-cancer.aspx

Old drug may teach new tricks in treating infectious diseases, cancer http://today.agrilife.org/2013/10/30/old-drug-may-teach-new-tricks-in-treating-infectious-diseases-cancer/

Meclizine inhibits mitochondrial respiration through direct targeting of cytosolic phosphoethanolamine metabolism. http://www.ncbi.nlm.nih.gov/pubmed/24142790

We recently identified meclizine, an over-the-counter drug, as an inhibitor of mitochondrial respiration. Curiously, meclizine blunted respiration in intact cells but not in isolated mitochondria, suggesting an unorthodox mechanism. Using a metabolic profiling approach, we now show that treatment with meclizine leads to a sharp elevation of cellular phosphoethanolamine, an intermediate in the ethanolamine branch of the Kennedy pathway of phosphatidylethanolamine biosynthesis. Metabolic labeling and in vitro enzyme assays confirmed direct inhibition of the cytosolic enzyme CTP:phosphoethanolamine cytidylyltransferase (PCYT2). Inhibition of PCYT2 by meclizine led to rapid accumulation of its substrate, phosphoethanolamine, which is itself an inhibitor of mitochondrial respiration. Our work identifies the first pharmacologic inhibitor of the Kennedy pathway, demonstrates that its biosynthetic intermediate is an endogenous inhibitor of respiration, and provides key mechanistic insights that may facilitate repurposing meclizine for disorders of energy metabolism.

Methods and compositions for treating degenerative and ischemic disorders http://www.google.com/patents/US20120136007

Model systems have shown that shifting a cell’s reliance from oxidative phosphorylation (OXPHOS) to glycolysis can protect against cell death. Exploiting the therapeutic potential of this strategy, however, has been limited by the lack of clinically safe agents that remodel energy metabolism. The present invention identifies non-toxic small molecules (e.g., drug-like compounds) that are capable of modulating oxidative metabolism. One identified compound comprises meclizine. As described herein, meclizine, and its enantiomer S-meclizine, redirects OXPHOS to glycolysis. Such compounds could be protective or therapeutic in degenerative disorders such as diabetes, Huntington’s, Parkinson’s, and Alzheimer’s disease and/or ischemic disorders including, but not limited to, stroke, heart attack, or reperfusion injuries.

Induction of apoptosis and cell-cycle arrest in human colon cancer cells by meclizine http://mts.tmu.edu.tw/BreastCancer/files/writing_journal/4/19_7ad05164.pdf

Meclizine (MEC), a histamine H1 antagonist, is used for the treatment of motion sickness and vertigo. In this study, we demonstrate that MEC dose-dependently induced apoptosis in human colon cancer cell lines (COLO 205 and HT 29 cells). Results of a DNA ladder assay revealed that DNA ladders appeared with MEC treatment in COLO 205 cells at dosage of >50 lM. In addition, the total cell number decreased dose-dependently after treatment with MEC in COLO 205 and HT 29 cells. Using flow cytometry, the percentage of COLO 205 cells arrested at G0/G1 phase increased dose-dependently. Analysis of changes in cell-cycle arrest-associated proteins with Western blotting showed that p53 and p21 were upregulated after treatment with MEC. The kinase activities of cyclin-dependent kinase 2 (CDK2) and CDK4 were suppressed in MEC-treated cells. As for apoptosis, MEC may induce upregulation of p53 and downregulation of Bcl-2, thus causing the release of cytochrome C from mitochondria and the translocation of apoptosis-inducing factor (AIF) to the nucleus. This resulted in the activation of caspase 3, 8, and 9. Our results provide the molecular basis of MEC-induced apoptosis and cell-cycle arrest in human colon cancer cells

Synthetic phosphoethanolamine induces cell cycle arrest and apoptosis in human breast cancer MCF-7 cells through the mitochondrial pathway. http://www.ncbi.nlm.nih.gov/pubmed/23773853

Phosphoethanolamine (Pho-s) is a compound involved in phospholipid turnover, acting as a substrate for many phospholipids of the cell membranes. In a recent study, we showed that Pho-s has antitumor effect in the several tumor cells. In this study we evaluated the antitumor activity of synthetic Pho-s on MCF-7 breast cancer cells. Here we demonstrate that Pho-s is cytotoxic to MCF-7 cells in a dose-dependent manner, while it is cytotoxic to MCF10 only at higher concentrations. In addition, Pho-s induces a disruption in mitochondrial membrane potential (Δψm). Furthermore, Pho-s induces mitochondria aggregates in the cytoplasm and DNA fragmentation of MCF-7 cells visualized by confocal microscopy. In agreement with the reduction on Δψm, we showed that Pho-s induces apoptosis followed by an increase in cytochrome c expression and capase-3-like activity in MCF-7 cells. Our results demonstrate that Pho-s induces a cell cycle arrest in the G1 phase through an inhibition of cyclin D1 and stimulates p53. An additional highlight of this study is the finding that Pho-s inhibits Bcl-2, inducing apoptosis through the mitochondrial pathway. Taken together, these results show that Pho-s is a promising compound in the fight against cancer.

Anti-angiogenic and anti-metastatic activity of synthetic phosphoethanolamine. http://www.ncbi.nlm.nih.gov/pubmed/23516420

BACKGROUND: Renal cell carcinoma (RCC) is the most common type of kidney cancer, and represents the third most common urological malignancy. Despite the advent of targeted therapies for RCC and the improvement of the lifespan of patients, its cost-effectiveness restricted the therapeutic efficacy. In a recent report, we showed that synthetic phosphoethanolamine (Pho-s) has a broad antitumor activity on a variety of tumor cells and showed potent inhibitor effects on tumor progress in vivo.

METHODOLOGY/PRINCIPAL FINDINGS: We show that murine renal carcinoma (Renca) is more sensitive to Pho-s when compared to normal immortalized rat proximal tubule cells (IRPTC) and human umbilical vein endothelial cells (HUVEC). In vitro anti-angiogenic activity assays show that Pho-s inhibits endothelial cell proliferation, migration and tube formation. In addition, Pho-s has anti-proliferative effects on HUVEC by inducing a cell cycle arrest at the G2/M phase. It causes a decrease in cyclin D1 mRNA, VEGFR1 gene transcription and VEGFR1 receptor expression. Pho-s also induces nuclear fragmentation and affects the organization of the cytoskeleton through the disruption of actin filaments. Additionally, Pho-s induces apoptosis through the mitochondrial pathway. The putative therapeutic potential of Pho-s was validated in a renal carcinoma model, on which our remarkable in vivo results show that Pho-s potentially inhibits lung metastasis in nude mice, with a superior efficacy when compared to Sunitinib.

CONCLUSIONS/SIGNIFICANCE: Taken together, our findings provide evidence that Pho-s is a compound that potently inhibits lung metastasis, suggesting that it is a promising novel candidate drug for future developments.

Synthetic phosphoethanolamine a precursor of membrane phospholipids reduce tumor growth in mice bearing melanoma B16-F10 and in vitro induce apoptosis and arrest in G2/M phase. http://www.ncbi.nlm.nih.gov/pubmed/22902646

Phosphoethanolamine (Pho-s) is a compound involved in phospholipid turnover, acting as a substrate for many phospholipids of the cell membranes, especially phosphatidylcholine. We recently reported that synthetic Pho-s has potent effects on a wide variety of tumor cells. To determine if Pho-s has a potential antitumor activity, in this study we evaluated the activity of Pho-s against the B16-F10 melanoma both in vitro and in mice bearing a dorsal tumor. The treatment of B16F10 cells with Pho-s resulted in a dose-dependent inhibition of cell proliferation. At low concentrations, this activity appears to be involved in the arrest of the cell cycle at G2/M, while at high concentrations Pho-s induces apoptosis. In accordance with these results, the loss of mitochondrial potential and increased caspase-3 activity suggest that Pho-s has dual antitumor effects; i.e. it induces apoptosis at high concentrations and modulates the cell cycle at lower concentrations. In vivo, we evaluated the effect of Pho-s in mice bearing B16-F10 melanoma. The results show that Pho-s reduces the tumoral volume increasing survival rate. Furthermore, the tumor doubling time and tumor delays were substantially reduced when compared with untreated mice. Histological analyses reveal that Pho-s induces changes in cell morphology, typical characteristics of apoptosis, in addition the large areas of necrosis correlating with a reduction of tumor size. The results presented here support the hypothesis that Pho-s has antitumor effects by the induction of apoptosis as well as the inhibition of cell proliferation by arrest at G2/M. Thus, Pho-s can be regarded as a promising agent for the treatment of melanoma.

Fosfoetanolamina cura mesmo o c¢ncer de pacientes humanos? TRUCO! Quero ver para crer!

Fosfoetanolamina no tratamento de c¢ncer

Master thesis of dr. Renato Meneguelo, 2007: https://aminer.org/archive/53e9bd5ab7602d97049f4e7b

Metabolomics identifies the intersection of phosphoethanolamine with menaquinone-triggered apoptosis in an in vitro model of leukemia. http://www.ncbi.nlm.nih.gov/pubmed/26175011

Altered metabolism is increasingly acknowledged as an important aspect of cancer, and thus serves as a potentially fertile area for the identification of therapeutic targets or leads. Our recent work using transcriptional data to predict metabolite levels in cancer cells led to preliminary evidence of the antiproliferative role of menaquinone (vitamin K2) in the Jurkat cell line model of acute lymphoblastic leukemia. However, nothing is known about the direct metabolic impacts of menaquinone in cancer, which could provide insights into its mechanism of action. Here, we used metabolomics to investigate the process by which menaquinone exerts antiproliferative activity on Jurkat cells. We first validated the dose-dependent, semi-selective, pro-apoptotic activity of menaquinone treatment on Jurkat cells relative to non-cancerous lymphoblasts. We then used mass spectrometry-based metabolomics to identify systems-scale changes in metabolic dynamics that are distinct from changes induced in non-cancerous cells or by other chemotherapeutics. One of the most significantly affected metabolites was phosphoethanolamine, which exhibited a two-fold increase in menaquinone-treated Jurkat cells compared to vehicle-treated cells at 24 h, growing to a five-fold increase at 72 h. Phosphoethanolamine elevation was observed prior to the induction of apoptosis, and was not observed in menaquinone-treated lymphoblasts or chemotherapeutic-treated Jurkat cells. We also validated the link between menaquinone and phosphoethanolamine in an ovarian cancer cell line, suggesting potentially broad applicability of their relationship. This metabolomics-based work is the first detailed characterization of the metabolic impacts of menaquinone treatment and the first identified link between phosphoethanolamine and menaquinone-induced apoptosis.

Distinct metabolic responses of an ovarian cancer stem cell line http://bmcsystbiol.biomedcentral.com/articles/10.1186/s12918-014-0134-y

One metabolite identified as significantly different in OCSCs, phosphoethanolamine, is a substrate for many cell membrane phospholipids that has recently been shown to induce both cell cycle arrest and apoptosis in cancer cells [15,16]. Here, intracellular phosphoethanolamine levels for OCSCs (and OCCs even though it is not a significant effect) stay fairly consistent over 48 hours for the control cells, but for the metabolic perturbations, the levels steadily increase over 48 hours. Because the phosphoethanolamine levels increase slightly but consistently for all metabolic perturbations, the reaction seems to be a generalized metabolic stress response. This reaction could be indicative of increased phospholipid membrane turnover or an apoptotic response to the increasing stress levels.

According to the lawyer of Blumenau Rubens Garcia in June and July, customers receive 180 capsules, then started receiving 120 and the new grant injunctions only 60. As the intake is one capsule a day, before shipment that lasted half a year currently serves each patient for only two months. (Ref)

Disclaimer:

This site is not designed to and does not provide medical advice, professional diagnosis, opinion, treatment or services to you or to any other individual. Through this site and linkages to other sites, I provide general information for educational purposes only. The information provided in this site, or through linkages to other sites, is not a substitute for medical or professional care, and you should not use the information in place of a visit, call consultation or the advice of your physician or other healthcare provider. I am not liable or responsible for any advice, course of treatment, diagnosis or any other information, services or product you obtain through this site. This is just my own personal opinion regarding what we have learned on this road.

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