Chloroquine & Hydroxychloroquine: supporting chemo effectiveness and more


Chloroquine is an anti-malarial drug available at pharmacies for people travelling to area with malaria risks as well as to address other health challenges.

Note: based on a RGCC chemosensitivity analysis I have seen at a German clinic, Hydroxychloroquine has been effective in killing the cancer cells of 5 out 7 patients that were tested.

It is one of very few available drugs that inhibits autophagy, a mechanism associated with its anticancer properties. However, note that Chloroquine has other properties as well that may be very well related to anti cancer mechanism, such as zinc ionophore, and others (see below the section on mechanisms).

In cancer, authophagy is the process used by cancer cells to “self-eat” in order to survive. This is why authophagy can be both good and bad. Specifically, if authophagy is prolonged this will become a lethal process to cancer. On the other hand, for a short while (e.g. during chemotheraphy, radiotheraphy, etc.) authophagy is used by cancer cells to survive. Indeed, one of the mechanisms responsible for survival of the therapy-resistant hypoxic cells is (macro-) autophagy: a phenomenon in which cells provide themselves with energy (ATP) by digesting their own cell-organelles.

Therefore, if we can induce somehow a sustained authophagy process, theoretically cancer cells will end up consuming themselves and finally tumors will be gone. However, in realty I think this is challenging to achieve. What we can do on the other hand is to attack cancer cells with various treatments such as Salinomycin, 3BP, Diflunisal, B17, Chemotheraphy, Radiotheraphy, Vitamin C, etc. while starving the cancer cells via e.g. diet and medication, and at the same time use Chloroquine to inhibit the process through which the cancer cells will try to eat themselves during the treatment in order to survive. Indeed, Chloroquine is a potent blocker of autophagy and has been demonstrated in a lab setting to dramatically enhance tumor response to radiotherapy, chemotherapy and even anti-hormonal therapy (please see references below).

This is why Chloroquine has become part of  many clinical trials, in combination with chemotherapy and other form of cancer treatments. The results are promising: “The results are very encouraging — striking, even says senior author Ravi Amaravadi, MD, an assistant professor of Medicine at Penn’s Abramson Cancer Center. Temsirolimus by itself has little effect in this patient population. Tumors laugh at it, with response percentages of just zero to 5 percent. But by combining it with hydroxychloroquine, we found that 14 out of 21 patients had stable disease after treatment, including five out of six melanoma patients.” (Ref1) 

Its anticancer properties are relevant for most cancers. Therefore, this drug can be part of an anti-cancer drug cocktail and I would consider it as an addition next to chemo and/or radiation treatment. However, whenever considering to add to a chemo treatment just perform a short google check of the specific chemo and Chloroquine combo to make sure there is no study indicating antagonism.

Update April 22nd 2018: Another anti-malaria drug called Amodiaquine, seems to be even more effective than Chloroquine/ Hydroxychloroquine

Update August 1st 2019: Due to it’s antithrombotic, vascular protective, immunomodulatory, improved glucose tolerance, lipidlowering and anti-infectious activity, Hydroxychloroquine will be used in French hospitals to possibly induce prevention of recurrent miscarriage (Ref.).

Update March 12th, 2020: Hydroxychloroquine has been shown to be effective against Coronavirus.

More specifically, there are several scientific publications indicating that:

Case Reports and Clinical Trials in Cancer

Update Dec 2019: Case report: stage 4 pancreatic cancer to remission using paricalcitol and hydroxychloroquine in addition to traditional chemotherapy by Stephen Bigelsen: I am a physician specializing in Allergy and Asthma, who in July 2016, had tumors in the head and the tail of the pancreas with scattered peritoneal metastases and a CA19-9 of 11,575 U/mL. Working with physicians from Weill-Cornell and Johns Hopkins, I began treatment with gemcitabine and capecitabine, plus IV Paricalcitol (25 mcg 3x’s/week) and hydroxychloroquine (600 mg BID). These are both safe and inexpensive treatment options that have shown success in pre-clinical models, phase 2 human trials, and are readily available. I have now enjoyed a complete response with my latest CA19-9 of just 15 U/mL and no evidence of active disease on my most recent CT scan.

Hydroxychloroquine in Previously Treated Patients With Metastatic Pancreatic Cancer Hydroxychloroquine is approved for the treatment of non-cancerous illnesses such as rheumatoid arthritis and systemic lupus erythematous. Researchers in the laboratory have tested tumors from patients with pancreatic cancer and have discovered that they have certain pathways inside the cells that promote growth and survival of the tumor. Hydroxychloroquine may inactivate these pathways and results in the death of pancreatic cancer cells.

Hydroxychloroquine in Metastatic Estrogen Receptor-Positive Breast Cancer Progressing on Hormonal Therapy

Hydroxychloroquine With or Without Erlotinib in Advanced Non-small Cell Lung Cancer (NSCLC)

Ixabepilone and Hydroxychloroquine in Treating Patients With Metastatic Breast Cancer

Docetaxel and Hydroxychloroquine in Treating Patients With Metastatic Prostate Cancer

Here is a longer list of clinical trials including Hydroxychloroquine: List


  • Endosomal Acidification Inhibitor: Chloroquine is a lysosomotropic agent that prevents endosomal acidification [1]. It accumulates inside the acidic parts of the cell, including endosomes and lysosomes. This accumulation leads to inhibition of lysosomal enzymes that require an acidic pH, and prevents fusion of endosomes and lysosomes. Chloroquine is commonly used to study the role of endosomal acidification in cellular processes, such as the signaling of intracellular TLRs. Moreover, Chloroquine inhibits autophagy as it raises the lysosomal pH, which leads to inhibition of both fusion of autophagosome with lysosome and lysosomal protein degradation.
    Trapped as cationic species in the acidic organelles owing to his basic pKa, thereby elevating the endosomal pH.
    It disburses quickly throughout the body and tends to reside primarily in the lysosomes, the so-called digestive organelles of cells. Lysosomes are involved with how cells dispose of waste material, including from the cell itself. In that role, they are important in the process of autophagy, where a cell under stress in desperate need of nutrition begins to feed upon itself. Autophagy is one way of killing cancer cells. Ref.
  • Chloroquine is a zinc ionophore.
  • May also interfere with Iron:
  • Chloroquine is a 4-aminoquinilone. The 4-aminoquinolones act by intercalation into the DNA of parasites
  • Another proposed mechanism involves breakdown of hemoglobin by the parasite and binding of chloroquine to ferriprotoporphyrin IX causing membrane damage.
  • Lowers intracellular pH and increases Ca release in cytoplasm from intracellular organelles: “When parasites are exposed to chloroquine, the cytosolic pH decrease as a result of extrusion of protons from acidic compartments and the parasites (P. falciparum) try to restore the cytosolic pH level using plasma membrane mechanisms (Saliba & Kirk 1999, Marchesini et al. 2000, Saliba et al. 2003). By using microphysiometry we showed that addition of chloroquine to P. chabaudi at the trophozoite stage led to a dose-dependent increase in the extracellular acidification rate (Fig. 6). The mean 50% maximal effective concentration (EC50) for three experiments was 16.29 ± 0.4 µM (n = 3) of chloroquine. This data reveal an activation of plasma membrane mechanism of protons extrusion under chloroquine treatment.”
    “We have previously shown that the acidic pool also functions as a Ca2+ store in permeabilized malaria parasites and that chloroquine causes Ca2+ release from this store (Passos & Garcia 1998). In the present study, intact parasites were labeled with the calcium indicator, Fluo-3 AM to measure parasite cytosolic Ca2+ mobilization, and we also investigated the acidic pools in intact parasites within the RBC, using confocal microscopy.” Ref 


Although in theory the side effects can be multiple, this drug is used by many people while traveling in countries with malaria risks.

The potential side effects include gastrointestinal disorders, headache, dizziness, non-retinal eye problems, hearing loss, rash.
To my knowledge, one of the serious side effects is that in relation to retinopathy that may occur when used for long time. However, from various studies retinopathy was unlikely to occur with HCQ at dosages less than 6.5mg/kg body weight with less than 10 years of treatment. On the other hand, high dose (1000 mg daily) hydroxychloroquine can lead to retinal toxicity in less than 6 months administration (Ref).
Since it is far less toxic to the retina, hydroxychloroquine has replaced chloroquine.

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Preparation & Administration

Hydroxychloroquine comes in 200 mg tablets and is taken orally. The dose provided will be based upon a calculation of 6.5 mg/kg (subject’s weight), which is the dose range commonly used to treat rheumatoid arthritis and lupus. Dosages will be rounded to the nearest 100 mg. Taken orally once a day. Administration during or after meals. (6.5 mg/kg will lead to about 400mg/day for most people.)

Some clinical trials are increasing the daily dose up to 1000mg but I woudl not go that high. The highest I would go would probably be 600mg/day.

Adding Zinc may  help: We report that chloroquine is a zinc ionophore, which targets zinc to the lysosomes, and that the combination of zinc and chloroquine enhances their cytotoxicity and induces apoptosis in a human cancer cell model system Ref.

Note: hydroxycloroquine has a long half-life (32-56 days) in blood and a large volume of distribution (Ref). In other words, the max time required to be totally out of the blood may be up to 112 days!

Source & Cost

Other Name: Plaquenil, etc.

Can be ordered from pharmacy including online pharmacies such as this one. Here you have to say that you are going to a country like Haiti and pick a specific location in that country using Google maps as they will check that, 6 months trip should be equal with about 6 boxes for one person.

There are many pharmacies that are selling Chloroquine – so if you want it you will be able to find it at one of these pharmacies.

Synergists & Antagonists

Chloroquine can interact with Etoposide:

  • Indeed there is a study showing that Chloroquine stops the action of Etoposite in cells that are surrounded by normal pH (such as normal cells) and allows Etoposite to work in cells that are surrounded by acidic environment (such as cancer cells). So based on this, the authors suggest that Chloroquine could be used to lower the side effects of Etoposite (on normal cells) and be able to increase the dose of Etoposite and target better cancer cells.

Adding Zinc may  help: We report that chloroquine is a zinc ionophore, which targets zinc to the lysosomes, and that the combination of zinc and chloroquine enhances their cytotoxicity and induces apoptosis in a human cancer cell model system Ref.

Verapamil may enhance effectiveness by inhibiting Choloquine efflux from cancer cell:

Tetrandrine will do the same or better job as Verapamil at inhibiting MDR resistance

Chloroquine seems to work well with Salinomycin


Since you are here:

You may want to have a look at a summary of this website. You will find so many more interesting repurposed rugs for cancer


Researchers Say Malaria Drug Could Also Treat Cancer:

Autophagy as a target for cancer therapy: new developments

Autophagy is an evolutionarily conserved lysosomal degradation pathway that eliminates cytosolic proteins, macromolecules, organelles, and protein aggregates. Activation of autophagy may function as a tumor suppressor by degrading defective organelles and other cellular components. However, this pathway may also be exploited by cancer cells to generate nutrients and energy during periods of starvation, hypoxia, and stress induced by chemotherapy. Therefore, induction of autophagy has emerged as a drug resistance mechanism that promotes cancer cell survival via self-digestion. Numerous preclinical studies have demonstrated that inhibition of autophagy enhances the activity of a broad array of anticancer agents. Thus, targeting autophagy may be a global anticancer strategy that may improve the efficacy of many standard of care agents. These results have led to multiple clinical trials to evaluate autophagy inhibition in combination with conventional chemotherapy. In this review, we summarize the anticancer agents that have been reported to modulate autophagy and discuss new developments in autophagy inhibition as an anticancer strategy.

Chloroquine is a zinc ionophore.

Chloroquine is an established antimalarial agent that has been recently tested in clinical trials for its anticancer activity. The favorable effect of chloroquine appears to be due to its ability to sensitize cancerous cells to chemotherapy, radiation therapy, and induce apoptosis. The present study investigated the interaction of zinc ions with chloroquine in a human ovarian cancer cell line (A2780). Chloroquine enhanced zinc uptake by A2780 cells in a concentration-dependent manner, as assayed using a fluorescent zinc probe. This enhancement was attenuated by TPEN, a high affinity metal-binding compound, indicating the specificity of the zinc uptake. Furthermore, addition of copper or iron ions had no effect on chloroquine-induced zinc uptake. Fluorescent microscopic examination of intracellular zinc distribution demonstrated that free zinc ions are more concentrated in the lysosomes after addition of chloroquine, which is consistent with previous reports showing that chloroquine inhibits lysosome function. The combination of chloroquine with zinc enhanced chloroquine’s cytotoxicity and induced apoptosis in A2780 cells. Thus chloroquine is a zinc ionophore, a property that may contribute to chloroquine’s anticancer activity.

Chloroquine inhibits the intracellular multiplication of Legionella pneumophila by limiting the availability of iron. A potential new mechanism for the therapeutic effect of chloroquine against intracellular pathogens.

Chloroquine and ammonium chloride, by virtue of their basic properties, have been shown to raise endocytic and lysosomal pH and thereby interfere with normal iron metabolism in a variety of cell types, including mononuclear phagocytes. Cellular iron metabolism is of critical importance to Legionella pneumophila, an intracellular bacterial pathogen whose capacity to multiply in human mononuclear phagocytes is dependent upon the availability of intracellular iron. In view of this, we have studied the effects of chloroquine and ammonium chloride on L. pneumophila intracellular multiplication in human monocytes. Chloroquine, at a concentration of 20 microM, and ammonium chloride, at a concentration of 20 mM, inhibited L. pneumophila intracellular multiplication by 1.4 +/- 0.2 (SEM) logs and 1.5 +/- 0.2 logs, respectively. Chloroquine- and ammonium chloride-induced inhibition of L. pneumophila intracellular multiplication was completely reversed by iron nitrilotriacetate, an iron compound which is soluble in the neutral to alkaline pH range, but not by iron transferrin, which depends upon acidic intracellular conditions to release iron. Chloroquine had no major direct effect on L. pneumophila multiplication in artificial media except at extremely high concentrations (15,000-fold that which inhibited L. pneumophila multiplication in mononuclear phagocytes), and inhibition at such concentrations was not reversed by iron nitrilotriacetate. This study demonstrates that chloroquine and ammonium chloride inhibit the intracellular multiplication of L. pneumophila by limiting the availability of iron to the bacterium. It is possible that such a mechanism of action underlies chloroquine’s antimicrobial effect against other intracellular pathogens, such as the agents of malaria and tuberculosis.

Acidic extracellular pH neutralizes the autophagy-inhibiting activity of chloroquine: implications for cancer therapies

Acidic pH is an important feature of tumor microenvironment and a major determinant of tumor progression. We reported that cancer cells upregulate autophagy as a survival mechanism to acidic stress. Inhibition of autophagy by administration of chloroquine (CQ) in combination anticancer therapies is currently evaluated in clinical trials. We observed in 3 different human cancer cell lines cultured at acidic pH that autophagic flux is not blocked by CQ. This was consistent with a complete resistance to CQ toxicity in cells cultured in acidic conditions. Conversely, the autophagy-inhibiting activity of Lys-01, a novel CQ derivative, was still detectable at low pH. The lack of CQ activity was likely dependent on a dramatically reduced cellular uptake at acidic pH. Using cell lines stably adapted to chronic acidosis we could confirm that CQ lack of activity was merely caused by acidic pH. Moreover, unlike CQ, Lys-01 was able to kill low pH-adapted cell lines, although higher concentrations were required as compared to cells cultured at normal pH conditions. Notably, buffering medium pH in low pH-adapted cell lines reverted CQ resistance. In vivo analysis of tumors treated with CQ showed that accumulation of strong LC3 signals was observed only in normoxic areas but not in hypoxic/acidic regions. Our observations suggest that targeting autophagy in the tumor environment by CQ may be limited to well-perfused regions but not achieved in acidic regions, predicting possible limitations in

Double autophagy modulators reduce 2-deoxyglucose uptake in sarcoma patients

The results of reduced SUVmax without tumor volume reduction after two weeks of Rapa and HCQ treatment may indicate that non-proliferative glycolysis occurred mainly in the cancer associated fibroblast compartment, and decreased glycolytic activity was evident from Rapa + HCQ double autophagy modulator treatment.

Autophagy as a modulator and target in prostate cancer

Autophagy, or ‘self-eating’, is an adaptive process that enables cells to cope with metabolic, toxic, and even infectious stressors. Although the adaptive capability of autophagy is generally considered beneficial, autophagy can also enhance nutrient utilization and improve growth characteristics of cancer cells. Moreover, autophagy can promote greater cellular robustness in the context of therapeutic intervention. In advanced prostate cancer, preclinical data provide evidence that autophagy facilitates both disease progression and therapeutic resistance. Notably, androgen deprivation therapy, taxane-based chemotherapy, targeted kinase inhibition, and nutrient restriction all induce significant cellular distress and, subsequently, autophagy. Understanding the context-dependent role of autophagy in cancer development and treatment resistance has the potential to improve current treatment of advanced prostate cancer. Indeed, preclinical studies have shown that the pharmacological inhibition of autophagy (with agents including chloroquine, hydroxychloroquine, metformin, and desmethylclomipramine) can enhance the cell-killing effect of cancer therapeutics, and a number of these agents are currently under investigation in clinical trials. However, many of these autophagy modulators are relatively nonspecific, and cytotoxicity in noncancerous tissues is still a concern. Moving forward, refinement of autophagy modulation is needed.

Targeting autophagy in breast cancer.

Macroautophagy (referred to as autophagy here) is an intracellular degradation pathway enhanced in response to a variety of stresses and in response to nutrient deprivation. This process provides the cell with nutrients and energy by degrading aggregated and damaged proteins as well as compromised organelles. Since autophagy has been linked to diverse diseases including cancer, it has recently become a very interesting target in breast cancer treatment. Indeed, current clinical trials are trying to use chloroquine or hydroxychloroquine, alone or in combination with other drugs to inhibit autophagy during breast cancer therapy since chemotherapy and radiation, regimens that are used to treat breast cancer, are known to induce autophagy in cancer cells. Importantly, in breast cancer, autophagy has been involved in the development of resistance to chemotherapy and to anti-estrogens. Moreover, a close relationship has recently been described between autophagy and the HER2 receptor. Here, we discuss some of the recent findings relating autophagy and cancer with a particular focus on breastcancer therapy.

The anti-malarial drug chloroquine sensitizes oncogenic NOTCH1 driven human T-ALL to γ-secretase inhibition.

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive cancer arising from T-cell progenitors. Although current treatments, including chemotherapy and glucocorticoids, have significantly improved survival, T-ALL remains a fatal disease and new treatment options are needed. Since more than 60% of T-ALL cases bear oncogenic NOTCH1 mutations, small molecule inhibitors of NOTCH1 signalling; γ-secretase inhibitors (GSI), are being actively investigated for the treatment of T-ALL. Unfortunately, GSI have shown limited clinical efficacy and dose-limiting toxicities. We hypothesized that by combining known drugs, blocking NOTCH activity through another mechanism, may synergize with GSI enabling equal efficacy at a lower concentration. Here, we show that the clinically used anti-malarial drug chloroquine (CQ), an inhibitor of lysosomal function and autophagy, decreases T-ALL cell viability and proliferation. This effect of CQ was not observed in GSI-resistant T-ALL cell lines. Mechanistically, CQ impairs the redox balance, induces ds DNA breaks and activates the DNA damage response. CQ also interferes with intracellular trafficking and processing of oncogenic NOTCH1. Interestingly, we show for the first time that the addition of CQ to γ-secretase inhibition has a synergistic therapeutic effect on T-ALL and reduces the concentration of GSI required to obtain a reduction in cell viability and a block of proliferation. Overall, our results suggest that CQ may be a promising repurposed drug in the treatment of T-ALL, as a single treatment or in combination with GSI, increasing the therapeutic ratio.


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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24 thoughts on “Chloroquine & Hydroxychloroquine: supporting chemo effectiveness and more

  1. I started to give Chloroquine to my mother today

    500mg Daily , she’s weight : 80Kg

    but i will change to HydroxyChloroquine soon

    Chemo alone is not effective , hope it will be better when adding Chloroquine to it , i will share the results next month

  2. Dear Daniel and All,
    I am very intrested in collodial silver and believing it.While searching unti-malaria drugs,i have found this video.
    In Gana,they use silver for malaria in hospitals.And it is working very fast.
    And silver is also very affective on warm,parasites,fungus etc..(now we are using drugs about them)
    And also it is synergetic with chemo on resistant cells on lab tests.Still i couldnt find any human result,accept my mother.
    Any idea?
    Kind Regards

    1. Hi Ergin,

      Thnaks. I will check the link this evening.
      Some one else that I very much trust, was very enthusiast after using on his mom colloidal silver IV.
      Simply because it is effective against parasites, etc. should help chemo if given the days prior to chemo.

      Kind regards,

      1. its tough how many anti parasite drugs and supplements are proven to have anti cancer properties.
        Hard not to think of cancer as a complicated parasite with innate components and a more complex adapting mechanism. Maybe standard chemoterapy should focus more on this nature too.
        On the other hand I also hypothyse that most stuff that can hurt an embryo would also have anti cancer properties. Think of thalidomide. Are there other good examples?

        1. list of drugs that are dangerous to an embryo follows below according to
          lots of these are used in anti cancer cocktails.
          maybe its an old analogue, sorry if it was obvious to the readers!!

          ACE (angiotensin converting enzyme) inhibitors such as:
          benazepril (Lotensin)
          captopril (Capoten)
          enalapril (Vasotec)
          fosinopril sodium (Monopril)
          lisinopril (Zestril, Prinivil)
          lisinopril + hydrochlorothiazide (Zestoretic, Prinzide)
          quinapril (Accupril)
          ramipril (Altace)
          Acne medication isotretinoin (Accutane, Retin-A)
          Alcohol — increases the risk of a stillbirth and the Fetal Alcohol Syndrome.
          Androgens (male hormones)
          Antibiotics tetracycline (Achromycin), and doxycycline (Vibramycin), metronidazole (Flagyl), and streptomycin
          Anticoagulant (blood-thinner) warfarin (Coumadin)
          Anticonvulsants (seizure medications) such as:
          phenytoin (Dilatin)
          valproic acid (Depakene, Valprotate),
          trimethadione (Tridione)
          paramethadione (Paradione)
          carbamazepine (Tegretol)
          Anti-depressant drug lithium (Eskalith, Lithob).
          Antimetabolite/anticancer drugs methotrexate (Rheumatrex) and aminopterin
          Antirheumatic agent and metal-binder (chelator) penicillamine (Ciprimene, Depen)
          Antithyroid drugs such as:
          thiouracil/propylthiouracil and
          DES (diethylstilbestrol), a hormone
          Thalidomide (Thalomid) which was approved by the FDA for the treatment of a complication of leprosy (erythema nodosum leprosum

        2. Yes, the parasites like to consume a lot of sugar themselves and they are usually eukaryotes (having a nucleus in the cell(s)) so they are closer to us genetically speaking than bacteria (to which cancer is also compared often). Is there a list somewhere of antiparasitic drugs that have been proven effective against cancer?

          Thanks in advance.

          1. hi Helga,
            i had mebendazole,Artemisin and Pyrivinium in mind but in a way we can add anti malaria drug chloroquine. im sure there are others. cheers

    2. Hi Ergin,

      Here is an article about anticancer effect of colloidal silver:

      Colloidal silver had dose-dependent cytotoxic effect in MCF-7 breast cancer cells through induction of apoptosis, shown an LD50 (3.5 ng/mL) and LD100 (14 ng/mL) (*P < 0.05), significantly decreased LDH (*P < 0.05) and significantly increased SOD (*P < 0.05) activities. However, the NO production, and Gpx, CAT, and Total antioxidant activities were not affected in MCF-7 breast cancer cells. PBMC were not altered by colloidal silver.


      The present results showed that colloidal silver might be a potential alternative agent for human breast cancer therapy.

      An article in a British newspaper:

      The usual naysayers:
      "Colloidal silver isn't considered safe or effective for any of the health claims manufacturers make. Silver has no known purpose in the body. Nor is it an essential mineral, as some sellers of silver products claim."

      These people would have no qualms nevertheless to put platinum (e.g. cisplatin) in your body in the form of a very toxic chemo or even mercury (in vaccines). Do those have any role in the body? No…. But … you know.

      Another notorious website, notorious for rejecting everything not in the mainstream:

      At least you can learn from it that once you turn blue from colloidal silver you might have ingested too much.


      Broad-spectrum bioactivities of silver nanoparticles: the emerging trends and future prospects

      There are alarming reports of growing microbial resistance to all classes of antimicrobial agents used against different infections. Also the existing classes of anticancer drugs used against different tumours warrant the urgent search for more effective alternative agents for treatment. Broadspectrum bioactivities of silver nanoparticles indicate their potential to solve many microbial resistance problems up to a certain extent. The antibacterial, antifungal, antiviral, antiprotozoal, acaricidal, larvicidal, lousicidal and anticancer activities of silver nanoparticles have recently attracted the attention of scientists all over the world. The aim of the present review is to discuss broad-spectrum multifunctional activities of silver nanoparticles and stress their therapeutic potential as smart nanomedicine. Much emphasis has been dedicated to the antimicrobial and anticancer potential of silver nanoparticles showing their promising characteristics for treatment, prophylaxis and control of infections, as well as for diagnosis and treatment of different cancer types.

      And what does Memorial Sloan Kettering Cancer Center say?

      Again, so much negativity and the same kind of nonsense as on the Mayo Clinic's website (see above):

      "Colloidal silver consists of silver particles suspended in a liquid. It is often produced by home-made generators. The use of silver medicinals to treat disorders such as epilepsy, gonorrhea, and colds was not uncommon until the mid-20th century. However, silver was replaced by safer therapies in the recent decades. Silver is not an essential mineral and does not serve any physiological function in the body. It denatures proteins by binding to their reactive groups and can inactivate some enzymes by forming hemisilver sulfides with sulfhydryl groups of the enzymes (1). Whereas silver compounds are still used in external preparations as antiseptics, there has been a growing interest in using the colloidal form of silver orally as an alternative medicine. In vitro studies indicate antitumor effects (8), but no human clinical data support the use of oral colloidal silver. However, despite lack of evidence, it is being promoted as a cure for AIDS, cancer, and diabetes.

      When taken orally, silver can interact with and reduce the effectiveness of tetracycline, quinolone, and penicillamine. Long term use can cause silver deposition in the skin and mucous membranes leading to an irreversible condition called argyria, characterized by bluish-gray to gray-black pigmentation (7). Other adverse effects include seizures (6) and kidney damage. Pregnant women should not consume colloidal silver as it can cause developmental abnormalities in the fetus (1)."

      What is particularly reprehensible that they dare to say that "silver was replaced by safer therapies in the recent decades". Nothing seems safer than colloidal silver. It is also telling that you have to accept a disclaimer (before you can access their page), which includes the following sentence: "Memorial Sloan Kettering Cancer Center makes no warranties nor express or implied representations whatsoever regarding the accuracy, completeness, timeliness, comparative or controversial nature, or usefulness of any information contained or referenced on this Web site." No accuracy can be expected! Basically they admit here that what they say is (or can be) rubbish. So much for a cancer center-published information. Draw your own conclusions.

      1. Hi Helga,

        Thank you for your very helpful post. Amazing that a Cancer Center is using such disclaimers. I can understand the need for disclaimers on sites like ours here since we are not trained in the medical field, etc., but not from a Cancer Center that is actually paid by society to be a professional in the field and represent the highest level of accuracy.

        Kind regards,

        1. Hi Daniel,

          Great to see my post didn’t get lost in the end! How did you resurrect it? I noticed Wondering also posted something to comment the same comment I was trying to and I thought that might be the reason my post was just hanging there, without appearing on your site.

          You are right, a taxpayer-funded cancer center should be held more responsible for what it states on its website than a citizen initiative like yours. Millions of heavy dollars go into the pockets of Sloan Kettering. I was asked to fill in a questionnaire so in the end I told them this reflects badly on them.

          I never tried colloidal silver before but maybe I’ll look into it myself.

          Kind regards,

    3. Hi Ergin, i just wrote a long comment on colloidal silver but the site doesn’t let me submit it. It does but doesn’t publish it, sadly. The window is still open but as with the mouse I cannot copy and paste it, it will be lost sadly.

      Anyway, I’m trying to at least copy the links here:
      don’t trust this site:
      same nonsense here:
      also here:

      Good sites:
      and this:
      and this:

      Click on the links and you’ll see.

      Best regards,

      1. Thank you very much Helga,
        When you enter a subject ,i am very happy.Because i know that you will search from begining to end.
        But when you enter silver subject it takes too many time,and i gave lots of time on silver and i am lost because of knowlodge pollution.

        I have very positive experiences with silver but didnt tell people to try.
        Our physcology is very different here.When there is no responce to chemo all life is changing.
        So now my researching is totally changed.Before i was searching for what kills cancer without chemo.
        Now i am searching for what is synergetic with chemo.Because i saw no positive happening without chemo.
        I know that silver doesnt work standalone,also silver+dca doesnt work.
        Also CHEMO+dca+hca+metformin+iv curcumin+quercetin+artemisinin++++ doesnt work for us.
        Only silver+chemo+others worked for my opinion.
        But now we began drugs which kills parasites+ others which helps chemo.May be we will see good responce on coming days with Daniels perfect job(T4 depletion).
        Kind Regards

        1. Hi Ergin,

          Thanks for the kind words. Silver is very difficult for an organism to process and there are only a few, mostly microorganisms, that can process it, biochemically speaking, which is one way they try to produce nano silver if I understand correctly. This might explain why it still works for your mom even though her cancer might be resistant to those that are inefficient.

          How about the Phlorizin? Has the doctor started treatment on her? Oh, gosh, I am not logged it, hope it will get through and Daniel can approve it.

          1. Dear Helga,
            Thanks Again
            While we were talking on Tetrathiomolybdate (TM),copper chelation,I wrote comments and give this link .But then i forget totally.

            Now i have a theory that silver chelated copper in my moms situation(She used it only 1 week).And worked for 2-3 weeks..
            Also in TM treatment ,when you stop drug,tumors grow rapidly more than before.Doubled in 1 week.
            Thats my theory,but not totally sure.But stg worked and this makes me feel alittle happy.Also we know that it helps chemo by killing parasites etc.
            I can switch to that protocol,if needed.
            Kind Regards

    1. Great to hear that Meech! Thank you!

      On the same line with our recent discussions, chloroquine is a base. As a result, for high glycolitic tumors, it will have difficulties getting to the cancer cells through the acidity surrounding the tumors

      This means that using proton pump inhibitors prior to chloroquine, as discussed here, it will increase the chance for its anti cancer effectiveness.

      1. Thanks for the information!

        I’ve been on a fairly low dose of a proton pump inhibitor for almost two weeks and have been considering stopping it due to DCA of course being acidic.

  3. Wanted to add this to the database for chloroquine effectiveness:
    Adding chloroquine to conventional treatment for glioblastoma multiforme: a randomized, double-blind, placebo-controlled trial.
    “In this single-center, randomized, double-blind, placebo-controlled trial, 30 patients receiving surgery, chemotherapy, and radiotherapy for glioblastoma multiforme were randomly assigned to receive chloroquine or placebo for 12 months. Median survival was 24 months for patients who received chloroquine and 11 months for patients who received placebo. No patient stopped therapy because of toxicity.”

  4. we have tried to use the HCL together with IE, starting HCL on 4th day (precaution) of IE (it is 5 days long) and tumor woke up (pain) started 5 days earlier than without HCL. for previous IE administrations pain usually started 1-3 days before the start of next chemo cycle but in this case it started 1 week prior to chemo.
    I can’t tell whether it was the IE-HCL interaction to blame or tumor developed resistance, but caution has to be taken for these 2 combination.
    Note – during chemotherapy no extracellular Ph adjustment was attempted.

    Appreciate if someone can share their experience about co-administration of HCL with Etoposide.

    1. @Daniel,
      This question is very important for me.
      Do you have a chance to ask those whom you know who use HCL for cancer treatment on daily basis for their experience on etoposide interaction? Do they increase the dose etoposide dose? or separate chemo and hcl administration in time?

      Thank you in advance


  5. Regarding autophagy, I read the following on Dr. Daniel Thomas’ blog. My question is – what kinds of substances eradicate senescent fibroblasts?

    “Increasing age is the most significant risk factor for the development of cancer, but why? Besides immune decline, chronological aging may enable the emergence of tumors through the onset of cell-cycle arrest (senescence) of aging fibroblasts. This makes fibroblasts prone to autophagy. Senescence-induced autophagy creates a permissive metabolic microenvironment for tumor initiation and growth through the production of high-energy mitochondrial fuels from fibroblasts (such as lactate) that feed nascent (emerging) cancer cells. Senescent fibroblasts can also stimulate tumor formation and promote its growth and spread through the production of inflammation-signaling molecules. To help prevent the onset or recurrence of cancer, we are pioneering the use of repurposed medicines, peptides, and natural compounds to eradicate aged, autophagy-prone, senescent fibroblasts.”

  6. I have a suspected tumor in upper esophagus(in the process of going to doctors). It recently started swelling rapidly and so I started taking metformin as well as several other herbs and pharmaceuticals including Hydroxychloroquine with zinc. It seems to be helping yet I came across this study cautioning against the combination of Metformin and Hydroxychloroquine.
    They seemed to indicate in an article reviewing the study that Metformin promoted autophagy while Hydroxychloroquine inhibited it causing problems in the cell.

    I know there is a link in the article under synergists and antagonists yet it doesn’t appear to be active any longer.

    Any thoughts would be greatly appreciated,

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