Anti Cholesterol Strategy to Fight Cancer


So far I wrote several posts that are in a way or another related to cholesterol & cancer, underlying the role of Cholesterol in cancer. More specifically, we have seen that drugs or supplements that reduce or inhibit the absorption, use and/or production of cholesterol in cancer cells, have also the potential to kill cancer cells: Ref.

Indeed, there are many scientific reports and review in the literature pointing towards the very important role of lipids in general (Ref.) and cholesterol specifically, in cancer (Ref.). Cholesterol has impact on oncogenic events, including tumor development, cell migration and angiogenesis (Ref.).

While going through the scientific literature I realized that one potential strategy to fight cancer is by focusing our treatment strategy towards depleting cholesterol available in cancer cells with as many tools as we have, and as coherent as we can, to address as many weak points as we can on the intra cellular cholesterol import or cholesterol production pathways.

So I though I should write a post that would consolidate the drugs and supplements I found relevant for this anti-cholesterol approach. I never found the time to do so, but recently, with the post from PaulF asking for ideas to fight lung cancer I though now is the moment to find time for this subject.

As it will be further discussed, this strategy is relevant for most of the cancers and even more for the hormone dependent cancers (e.g. prostate cancer, breast cancer, adrenal cancer, etc.), as it has the potential to also reduce hormone production.

Update November 2017: I must stress that here, we are speaking about intr-cellular cholesterol and not blood cholesterol only. As I will discuss below, blood cholesterol is only one piece of the cholesterol  puzzle. I am stressing this aspect, because I heard various cancer patients stating: “I have a good cholesterol  level” or “I never had problems with cholesterol” and based on this they conclude this strategy is not relevant for them. However, regardless of the blood cholesterol level, the intracellular cholesterol production and storage mechanisms are over active in most cancer-cell types and represent weak spots that can be targeted to fight cancer.

What is Cholesterol?

Cholesterol is a lipid molecule present in the membranes of all mammalian cells. It is essential for their growth and viability. As an indispensable constituent of plasma membranes, cholesterol affects properties and functions of membrane proteins such as receptors, enzymes, or ion channels. Next to this, cholesterol is the “fuel” required for hormone production in hormone producing cells.

What is the origin of Cholesterol?

Cells produce cholesterol or are able to draw it from extracellular sources via the LDL receptor (in this case coming from what we eat). Indeed, cells can also take up cholesterol from the body, transported by LDL and very-low-density lipoproteins (VLDL), to meet their cholesterol requirement. When cholesterol, PLs and TGs are in excess in the cells, they are exported into circulation as high-density lipoproteins (HDLs) or locally stored within the cell, as Lipid Droplets (Ref.)

Cholesterol produced inside the cell is based on acetyl coenzyme A (acetyl-CoA) which in turn is typically produced out of

  • Citrate, mainly coming out of mitochondria (produced from glucose or glutamine) (Ref.).
  • Acetate imported from outside the cell (Ref.). When cancer cells are deprived of essential nutrients they may also produce acetyl-CoA from acetate (Ref.).

Acetyl-CoA it is then taken up on the Mevalonate (MVA) pathway and finally converted into cholesterol and other components essential for normal cell function, but even more for tumor growth (Ref.). To understand this process a little better, you can have a look at this picture

From a cellular organelle point of view, the major site responsible for cholesterol synthesis is called the endoplasmic reticulum (ER) (Ref.).

To summarize the above, there are four major potential sources of cholesterol for the cell:

  • cholesterol from outside the cell coming from the body, including diet via the blood
  • cholesterol produced within the cell from imported glucose or glutamine
  • cholesterol produced within the cell from imported acetate
  • cholesterol previously stored within the cell as lipid droplets

What are the tumors we can fight with this anti-cholesterol strategy? 

Looking at the science, my answer to this question is essentially all cancers.

Here are a few examples taken from different perspective, connected with different cancers, but all pointing to the same direction, i.e. cholesterol is important fuel for tumor growth, and as a result a potential target to affect cancer cells:

Cholesterol from outside the cell: A HDL perspective

For example, the level of blood HDL can affect various cancers in various ways depending on whether HDL carries cholesterol away from them (which leads to anti cancer impact) or if HDL will actually carry towards them cholesterol (this is the case for some cancer cells expressing receptors that can interact with HDL, leading to tumor growth). Let’s discuss that a little:

Lipoproteins (LDL and HDL) transfer lipids (fats including cholesterol) around the body. LDL particles are sometimes referred to as bad cholesterol because they can transport lipid molecules around the body, into the cells (including artery walls, attract macrophages, and thus drive atherosclerosis). In contrast, HDL particles are often called good cholesterol or healthy cholesterol because they can remove lipid molecules (including cholesterol) from peripheral tissues and returns them to the liver for excretion or recycling. Indeed, HDL transports cholesterol mostly to the liver or steroidogenic organs such as adrenals, ovary, and testes by both direct and indirect pathways. (Ref.)

It has been shown that high HDL may be a good sign for some cancers (including that of lung (Ref.), Non-Hodgkin Lymphoma (Ref.) and others) and may be a bad sign for other cancers (including that of prostate (Ref.), breast (Ref.), ovary (Ref.) and others). The negative role of the “good cholesterol” in the tumors such as that of breast seems to be connected to HDL binding to SR-B1 and subsequent lipid transfer are sufficient to activate Src, which subsequently activates the PI3K/Akt and MAPK pathways. (Ref.). In other words, during the process of carcinogenesis, some tumor cells exploit the HDL mediated removal of cholesterol from peripheral tissues to satisfy their increased cholesterol requirements, via the overexpression of the scavenger receptor class B type 1 (SR-B1) receptor, to which HDL can connect.

It is interesting to realize, that most of those tumors for which HDL is not a good sign are possibly those of cells that typically produce hormones (including prostate, adrenal). In contrast, if the cell is only delivering cholesterol to HDL (and not receiving) that is good because cholesterol is being taken away. Regardless of the case, what we learn from here is that cholesterol in cancer cell is associated with progression.

Cholesterol transport inside the cell

Although HDL may also play that role for some cells, in general LDL is the main carrier for cholesterol around the body delivering cholesterol to the cells via LDL receptors, with a intracellular trajectory as discuses here Interfering with the intracellular cholesterol traffic is an important anti cancer strategy discussed in details in my post on Itraconazole (see link above). This approach is relevant for many cancers, and as a result is an important aspect to consider in an anti cholesterol strategy.

Cholesterol produced inside the cell: Mevalonate phatway

Therefore, when cells need cholesterol, one way for them to get that is increasing the expression of LDL receptors. However, when external supplies from e.g. diet cannot meet cell demands, mevalonate pathway (the main pathway responsible for cholesterol production out of acetyl-COA) becomes active and in cancers over active (Ref. and see references in the Reference section). I have discussed Mevalonate phatway and its inhibition in details here The modulation and inhibition of the activity of this pathways is known as an important target that should be considered in the fight against cancer (Ref.).

Cholesterol synthesis pathway

Cholesterol stored inside the cell: lipid droplets

As discussed in a previous post as well, when cancer cells have enough cholesterol available, they reduce LDL expression and start storing cholesterol as cholesteryl esters inside the cell (as cytoplasmic lipid droplets). To do this, cells need to use an enzyme called ACAT1 (acyl-coenzyme A (CoA):cholesterol acyltransferase), that converts cholesterol in its form that can be stored i.e. cholesteryl esters.

This storage of cholesterol has been shown to be very important for tumors such as pancreatic (Ref.), prostate (Ref.), breast (Ref.), adrenal and many others (Ref.) and the inhibition of storage potential by inhibiting ACAT1 may lead to cancer cell death.

Note that inhibition of MYC is accompanied by accumulation of intracellular lipid droplets in tumor cells as a direct consequence of mitochondrial dysfunction. This suggests that aggressive tumors use fatty acids as an energy source. MYC is a potent regulator of these processes by inducing increased glycolysis and glutaminolysis and by stimulating mitochondrial biogenesis and function (Ref.). Nitazoxanide is a MYC inhibitor (Ref.).

Cholesterol produced inside the cell: from ketone bodies and acetate

In cancer cells, ACAT1 has yet another important role besides cholesteryl esters storage. Indeed, it has been suggested that fibroblasts, with mitochondrial dysfunction, produce ketone bodies in the tumor stroma. These ketone bodies are imported via the MCT1 transporter (same transporter importing lactate and 3BP) and re-utilized by adjacent cancer cells, which process these ketone bodies as mitochondrial fuels for oxidative phosphorylation (OXPHOS), to drive anabolic tumor growth. In order to process ketone bodies, the expression of certain neuron-specific enzymes in cancer cells, such as ACAT1/2 would be required. (Ref.) This may also explain why tumors may still grow during restricted ketogenic diet. Although ketones would be restricted from an intake point of view, tumor micro environment will take care for the production of additional ketones to support tumor growth, yet probably a slower growth compared to when the tumor has the typical nutrients it needs.

Indeed, I also previously discussed this aspect indicating that when tumors are deprived of essential nutrients, Acetate is the fuel that finally can also represent fuel for cholesterol production. Mammalian cells express an enzyme, namely ACSS2, that catalyses synthesis of acetyl-CoA from acetate, and it is used to compensate for the loss of acetyl-CoA production by ACLY. It has been previously shown that the expression of ACSS2 is highly elevated upon ACLY suppression in all the cell lines tested. (Ref.) In general, conversion of acetate to acetyl-CoA is an energy-dependent process, whereas ACLY-dependent production of acetyl-CoA from glucose is an energy-producing reaction. This makes ACLY-dependent acetyl-CoA production pathway more preferable in mammalian cells, but the absence of ACLY may derive the cells toward ACSS2-dependent pathway. (Ref.)

Here is a nice map showing 3 major ways for intracellular acetyl-CoA production

And here is a book chapter discussing in details the Mevalonate Pathway including very useful charts: Reference

Consequently, this mechanism represents an important target in our anti-tumor strategy.

Strategy against cholesterol

In line with the above mechanism, here would be a coherent anti cholesterol strategy:

  1. reduce LDL carriers: this can be achieved with Niacin supplement (also called nicotinic acid or vitamin B1) (Ref.). The drawback is that HDL will be increased and that may not be good for some cancers. Therefore we need to check if our cancer is expected to show scavenger receptor class B type 1 (SR-B1) receptor. If yes, I would not use Niacin.
    • Dose: there is no specific dose described. Niacin dose is limited by its typical and harmless side effects known as flushing (Ref.)
    • Source: most online shops selling supplements – there is even a drug Niacor based on B1 but much more expensive compared to the supplement
  2. inhibit cholesterol absorption and or traffic by
    • blocking NPC1L1 gut transporters using Ezitimibe. Ezitimibe has been shown to also tumor angiogenesis in e.g. prostate cancer cells (Ref.). Indeed, it has been shown that high cholesterol induces angiogenesis and accelerates growth in e.g. breast tumors (Ref.) NPC1 can also be inhibited by Itraconazole
      • Dose & Source: see my post on Itraconazole at the link above
    • inhibiting ASM could be used to block intracellular cholesterol transport – Orally administered ASM inhibitors, perphenazine or fluphenazine, led to tumour inhibition but caused CNS-related sedation at concentrations required for anticancer activity. This was overcome by encapsulating the agents into nanoliposomes to modulate drug pharmacokinetics and potentially reduce blood–brain-barrier permeability (Ref.) Indeed, antipsychotics inhibit the cholesterol biosynthesis and reduce the lipoprotein-derived cholesterol trafficking to the cholesterol-regulated machinery in the ER. As a consequence, SREBP-1 and SREBP-2 are activated and the expression of genes involved in cholesterol and fatty acid metabolisms are stimulated (Ref.). This is why is good to always combine drugs such as those discussed in this section (inhibitors of cholesterol absorption and or traffic) with inhibitors of SREBP-1 and SREBP-2, discussed below (such as Metformin and Tocotrienols). SREBP-2 is the master regulator of cholesterol homeostasis.
  3. reduced Citrate conversion into acetyl-CoA that fuels the cholesterol production (mevalonate) pathway: use HCA supplement to inhibit ACLYL
    • Dose & Source: see my post on HCA at the link aboveAnother ACLY inhibitor is Bempedoic acid (ETC-1002), currently (2017) in clinical trials investigated as a potential drug to reduce reduced LDL-C in patients who cannot tolerate statins (Ref.). The drug is investigated by Esperion Therapeutics Inc., a late-stage pharmaceutical company.
    • Bempedoic acid is another ACLYL inhibitor in clinical trials, focused on lowering cholesterol level as an alternative to Statins
  4. inhibit cholesterol production (mevalonate) pathway: use Statins (that inhibit HMG-CoA reductase (HMGCR)) and possibly bisphosphonates.  Indeed recent research indicates that “Statin and Bisphosphonate Induce Starvation in Fast-Growing Cancer Cell Lines“. Specifically, I would chose a Lipophilic statins as those have been shown to be the most active (see Reference section as well as my recent post on Statins). Omega-3 also lowers intracellular cholesterol production via a direct inhibition of HMGCR (Ref.). Brutieridin and Melitidin, two statin-like flavanone inhibitors of HMGR, extracted from Bergamot fruit, exert a similar behavior with respect to the commercial statins (Ref.). Pu-erh tea leaves contains Lovastatin and can be found as food supplement capsules (Ref.).
    • Dose of statins: typical dose used to lower cholesterol (see drug indications)
    • Source: any pharmacy
    • Note: side effect of statins is CoQ10 deficiency
    • Note: Coadministration of simvastatin (or lovastatin) with antifungals (itraconazole or ketoconazole) can result in rhabdomyolysis and acute renal failure (Ref.) Simvastatin & lovastatin should therefore not be used concomitantly with itraconazole and other potent CYP3A4 inhibitors, or the dosage of lovastatin should be greatly reduced while using a CYP3A4 inhibitor (Ref.). This increased toxicity is not apparent with fluvastatin (Ref.)
    • Update August 7th 2019: To chose the right Statin and administration procedure please read this post I wrote recently
    • Update August 7th 2019: Prednisolone may further help to reduce the levels of HMGCR enzyme (this is the target of Statins) and FDPS enzyme (this is the target of Bisphosphonates) and this more effectively inhibit the mevalonate pathway (Ref.). This is why, this Nature paper has suggested the initiation of a clinical trial combining Statins+Bisphosponates+Prednisolone.
  5. Update: 10-April-2017: Tumor cells are sensitive to depletion of mevalonate-derived products but this activity triggers a homeostatic feedback loop that blunts statin efficacy. Dipyridamole inhibits this feedback response and potentiates statin antitumor activity (inhibiting the cleavage of SREBP2). So Dipyridamole is an important addition in order to maintain statins effectiveness (Ref.1, Ref.2).
    • Dose: 200mg 2 x day
    • Source: any pharmacy
      Note: Thank you to Frank Liu for heads up on this point via his comment.
  6. Update 01 Sept 2019: Inhibiting cholesterol production by inhibiting Lanosterol 14-alpha demethylase (CYP51) located downstream HMGR (Ref.), on the Post-Squalene pathways (Ref.). This can be inhibited by antifungals such as Itraconazole, Fluconazole, Miconazole, Ketoconazole (Ref.)
  7. inhibit storage of cholesterol as lipid droplets: use ACAT1 inhibitors such as Piperine, Honokiol, Omega 3, Ezitimibe, Sulfasalazine (all references at
    • Dose & Source: see my post on ACAT inhibitors at the link above
  8. reduce the import of acetate and ketone bodies by inhibiting MCT1-4 with NSAIDs such as Aspirin and/or Diclofenac and/or Quercetin. Some more MCTs inhibitors are discussed here
    • Dose: see the link above indicating typical dose used to inhibit MCTs
    • Source: any pharmacy as capsules, suppository or topical application
  9. Update: 10-April-2017: when ACLYL is inhibited by HCA, tumor cells will express ACSS2 enzyme to convert acetate into the actyl-CoA (Ref.). ACSS2 level is modulated by SREBP2 (Ref.) and SREBP2 in turn can be modulated by Vitamin E derivatives (tocotrienols) (Ref.). Apigenin also attenuates SREBP-2 (Ref.). According to malypaet (a contributor to this website) a spoon of fresh parsel by day would contain enough Apigenin to achieve the attenuation? (Ref.). Apigenin can also be found online as a supplement. ACLYL may also be inhibited by Omeprazole (Ref.).
    Update March 2020: Allicin (garlic extract) may be a good but reversible inhibitor of ACSS2 (Ref.)
    Interestingly, low extracellular pH also activates SREBP-2. Here is a very recent paper on that Therefore inhibiting glycolisis or proton pump transporters it is also a way to control SREBP-2. This finding is nice since it connects cholesterol biosynthesis with pH and glycolisis. The control of pH is discussed here
    As mentioned above, the HMG CoA reductase (HMGCR) activity is regulated by by the sterol regulatory element binding proteins (SREBPs) 1a and 2. However, in tumors HMGCR activity is elevated and resistant to sterol feedback regulation. But there is a secondary regulation, a nonsterol isoprenoid-mediated fine-tuning of reductase activity. This is why, isoprenoids including monoterpenes (carvacrol, L-carvone, geraniol, perillyl alcohol), sesquiterpenes (cacalol, farnesol, β-ionone), diterpene (geranylgeranyl acetone), “mixed” isoprenoids (tocotrienols), and their derivatives suppress the growth of tumor cells with little impact on non-malignant cells (Ref.1, Ref.2, Ref.3), inhibiting HMG CoA reductase via a secondary feedback loop. Ergosterol from edible mushroom also down regulates HMGCR (Ref.).
    In addition, isoprenoids such as perillyl alcohol may also inhibit the activity of geranylgeranyl-protein transferases (GGPTases) and farnesyl-protein transferase (FPTase), which are enzymes of the mevalonate pathway (Ref.1, Ref.2).
    Metformin also inhibits SREBP1 (Ref.).

    • Dose of isoprenoids: a suitable dose of tocotrienols seems to be 400 mg 2 x/day, and of lycopene about 120mg/day
    • Source: Online available supplements such as this one.
      Note: Thank you to Frank Liu for heads up on tocotrienols via this comment and to malypaet on Apigenin via this comment.
  10. Metformin should be a good addition to the above as it will slow down mitochondria and thus its output, Citrate, and in turn acetyl-CoA production out of glucose and glutamine. Next to that, Metformin also has the capability to reduce Mevalonate pathway activity, in a way similar to that of statins by inhibiting HMGCR (Ref.1, Ref.2, Ref.3). Indeed, Metformin significantly down-regulates cholesterol pathway genes (Ref.). Furthermore, Metfomin has been found to reduce LDL levels (Ref.1, Ref.2). It is indeed known, that adenosine monophosphate-activated protein kinase (AMPK), an energy sensor and central regulator of metabolism, downregulates the mevalonate pathway via phosphorylation (Ref.1, Ref.2) and transcriptional control (Ref.) of HMGCR. And so it makes sense that Metformin will affect mevalonate pathways, since it it a well known modulator of AMPK. Berberine is also a well known activator of AMPK (Ref.). Berberine is a natural supplement that is found at online shops and it is taken in a dose of about 1-2g/day.
    • Dose: typical Metformin target dose 1000mg to 2000mg/day, starting from 500mg and moving slowly up to the target dose
    • Source: any pharmacy
  11. Another point that could be addressed to further strengthen this strategy is related to Citrate. Citrate is absorbed from the blood via NaCT (PMCT or NaC2) transporter (Ref.). If HCA and/or Statins are not doing completely their job Citrate can be processed and become a source of cholesterol produced via Mevalonate pathway. In this case, cholesterol may be produced from Citrate in the liver (and released in the blood) or produced by the cancer cell itself. It is known that NaCT inhibitors might mimic caloric restriction, decrease fatty acid and cholesterol biosyntheses, prevent obesity, and extend life-span  (Ref.). However, I cannot find yet good inhibitors of NaCT. Only for NaDC-1 and NaDC-3, which is Lithium, but it will actually facilitate NaCT (Ref.)
    Update 16-Sept-2019: “a highly specialized plasma membrane protein (pmCiC, plamsamembranecitrate carrier) to be responsible for citrate uptake in cancer cells. PmCiC expression is detetcted in a wide variety of human cancer cell lines, as well as in human tumor tissue sections with differences in ex- pression levels among cancers, and within the different areas of individual cancers (invasion front and invading cells are often more stained that the cells in the central part of the tumor). The transporter is also present in normal prostate secretory cells (apically), but works in opposite directions, as citrate ex- porter, and is responsible for maintaining high extracellular citrate levels in the prostate gland” (Ref.) Here is the article that reports the finding (Ref.). In addition, this article also reports the discovery of Gluconate as a specific inhibitor of the pmCiC.

    • Source: I cannot find Gluconate alone as a supplement but Mg Gloconate or Zn Gluconate can be easily found
    • Dose of Gluconate: I would take 3x500mg/day of Mg Gluconate capsules (morning/afternoon/evening)

The above, next to a low cholesterol diet should be a good anti cholesterol strategy. Off-course, we will still use some fats in our diet and it is important not only to take care of the fat consumed but also its fatty acid composition (Ref.) as also discussed here

Notes on other “tools” that could contribute to the above strategy:

  • Tamoxifen works, in part, by reducing cholesterol (Ref.)
  • Green Tea inhibits cholesterol absorption (Ref.)
  • Cafe and Green Tea extract EGCG (Ref.)
  • Bergamot modulates cholesterol (Ref.)
  • Inhibitors of Squalene Synthase from Traditional Chinese Medicine (Ref.)
  • Flaxseed lignan extract SDG lowers cholesterol (Ref.)


Statin and Bisphosphonate Induce Starvation in Fast-Growing Cancer Cell Lines

Lipid metabolic reprogramming in cancer cells

Cholesterol Metabolism and Prostate Cancer Lethality.

The Contribution of Cholesterol and Its Metabolites to the Pathophysiology of Breast Cancer.

Why high cholesterol levels help hematological malignancies: role of nuclear lipid microdomains.

Lipid rafts as major platforms for signaling regulation in cancer.

Intratumor cholesteryl ester accumulation is associated with human breast cancer proliferation and aggressive potential: a molecular and clinicopathological study.

High ACAT1 expression in estrogen receptor negative basal-like breast cancer cells is associated with LDL-induced proliferation.

Lipid Droplets: A Key Cellular Organelle Associated with Cancer Cell Survival under Normoxia and Hypoxia.

Abrogating cholesterol esterification suppresses growth and metastasis of pancreatic cancer.

Targeting the SR-B1 Receptor as a Gateway for Cancer Therapy and Imaging.

SR-BI: Linking Cholesterol and Lipoprotein Metabolism with Breast and Prostate Cancer.

Comparison of expression and regulation of the high-density lipoprotein receptor SR-BI and the low-density lipoprotein receptor in human adrenocortical carcinoma NCI-H295 cells.

ACTH Regulation of Adrenal SR-B1.

Novel aspects of mevalonate pathway inhibitors as antitumor agents.

Effect of Lipophilic and Hydrophilic Statins on Breast Cancer Risk in Thai Women: A Cross-sectional Study.

Statin prescriptions and breast cancer recurrence risk: a Danish nationwide prospective cohort study.

Lovastatin lowers the risk of breast cancer: a population-based study using logistic regression with a random effects model.

Statins Dose-Dependently Exert Significant Chemopreventive Effects Against Various Cancers in Chronic Obstructive Pulmonary Disease Patients: A Population-Based Cohort Study.

Statin use and survival from lung cancer: a population-based cohort study.

Statin use after colorectal cancer diagnosis and survival: a population-based cohort study.

The effect of statins on survival in patients with stage IV lung cancer.

Statin Use and Its Impact on Survival in Pancreatic Cancer Patients.

Therapeutic Effects of Repurposed Therapies in Non-Small Cell Lung Cancer: What Is Old Is New Again

Extracellular Acidic pH Activates the Sterol Regulatory Element-Binding Protein 2 to Promote Tumor Progression.

Statins & Metformin Help Pancreatic Cancer Patients

Controlling cholesterol synthesis beyond 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR)

Additive antitumor effects of celecoxib and simvastatin on head and neck squamous cell carcinoma in vitro

Lipid-lowering statins as well as non-steroidal anti-inflammatory drugs (NSAIDs) have been reported to possess cancer-protective effects in many epidemiologic cohort studies. However, the underlying mechanisms of these findings are mostly unknown. To evaluate possible additive antitumor effects of statins and NSAIDs in vitro, PJ-41 and HLaC78 head and neck squamous cell carcinoma cells (HNSCC) were treated with 40 µM celecoxib, 50 µM simvastatin or a combination of both. Analysis of tumor viability, proliferation, apoptosis, cell cycle changes and secretion of interleukin-6 (IL-6) and interleukin-8 (IL-8) was conducted via MTT assay, Annexin V-propidium iodide test, cell cycle analysis, colony assay and enzyme-linked immunosorbent assay (ELISA). Celecoxib and simvastatin alone as well as a combined treatment showed a significant reduction in tumor cell viability, proliferation and secretion of IL-6 and IL-8 compared to the control group. The combined treatment even proved to have significantly greater effects. We postulate that simvastatin and celecoxib have additive antitumor effects on HNSCC in vitro, which warrants further investigation.

The combined administration of EGCG and caffeine induces not only suppression of fat accumulation but also anorexigenic action in mice

Polyunsaturated fatty acyl-coenzyme As are inhibitors of cholesterol biosynthesis in zebrafish and mice.

Biosynthesis of Cholesterol

The Potential of Isoprenoids in Adjuvant Cancer Therapy to Reduce Adverse Effects of Statins

Pathways of hepatic cholesterol and Coenzyme Q10 (CoQ10) biosynthesis in liver

Scheme of the mevalonate pathway and isoprenoid synthesis

Multivalent feedback regulation of HMG CoA reductase, a control mechanism coordinating isoprenoid synthesis and cell growth

Feedback Regulation of Cholesterol Synthesis

Atypical antipsychotics alter cholesterol and fatty acid metabolism in vitro

Cholesterol Trafficking: An Emerging Therapeutic Target for Angiogenesis and Cancer

Cholesterol Metabolism: A Potential Therapeutic Target in Glioblastoma

Omeprazole, an inhibitor of proton pump, suppresses De novo lipogenesis in gastric epithelial cells


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169 thoughts on “Anti Cholesterol Strategy to Fight Cancer

  1. Hi Daniel,
    Only i can say is excellent work,thanks.
    I find a very little time we are on treatments now.
    There is a correlation between albumin and cholosterol.
    And the ones who are on citric acid treatment should examin blood counts.
    Also hormones such as testosterone.
    Daniel solved this months ago but now i am learning.
    This is why Daniel asked Mr Halabe is there any cured patient who has ovarian cancer or prostate as i true remember.
    Kind Regards

  2. The more I learn about the disease, the more frustrating it gets. It seems like it can use way too many naturally occurring and biologically necessary substances for its purposes and that you have to get somewhat lucky to nail down a strategy which has a durable tumour shrinking effect.

    1. In the end we have to deal with the challenge of this humanity Meech. I wold put a different perspective to what you said: The more we learn the more we can work towards improving our outcome. Becoming aware that MCT1 manipulation may help the outcome in Ketogenic Diet (and not only), should help us put in place an improved strategy around KD. Next to that, we now realize that we have to do something also about the fibroblasts that are fueling the tumors with various nutrients. There is a drug from Japan that is effective against fibroblast and will write at some point about it. Besides that, here is a nice explanation showing that autophagy inhibitors such as Chloroquine can be very helpful against the process in which fibroblast are fueling tumors. So it should go nicely with KD. (I am referring to KD as I know you are doing that).
      And finally, fibroblasts are also the reason why some tumors can also grow without blood supply, explaining why in some tumors angiogenesis inhibitors may fail. But probably they should work very well with MCT1 inhibitors.

      1. Thanks for the post Daniel.

        So while inhibiting MCT1, would you avoid DCA? I saw that Quercetin is an inhibitor of MCT1 but that you would also advise against it being used with DCA.

        1. Very short but very good question Meech.
          There are two types of MCTs: proton dependent (MCT1-4) and sodium coupled (SMCTs). It its SMCT1 that is required for the access of DCA in the cell. Fortunately, there is one drug that can inhibit MCT1 (ref is in the article above) and upregulates SMCT1 (ref is in this post That is Diclofenac. That that may be an option, but off-course these NSAIDs all come with potential gastro intestinal side effects.
          If you remember, I mentioned that a friend with lung cancer was having pain and he didn’t wanted morfine. Instead he was taking a lot of Diclofenac while using DCA. His tumor was gone after that 🙂 He also used hyperthermia but it may also be the combination of DCA+Diclofenac?

          1. Thanks a lot for the information Daniel!

            I’ve read that taking PPIs along with Diclofenac can aleviate the GI symptoms and highly reduce risk of peptic ulcers so that would be something to consider.

            Unfortunately in Canada, Diclofenac is only available over the counter in topical gel form. I’ll have to find a way to get it prescribed to me.

    2. Indeed dear Meech, i kinda feel the same, but i tell you what. Ignorance is bliss. And in many situations i find that ignorant people survive more than others. Idiocracy? Who knows…. for sure.
      So in my ignorance, may i suggest more blood testing, immune system, hormones, minerals, vitamins, lipids, metals, proteins, markers etc etc etc
      Afterwards kinda give it your best to normalize levels with all tools at hand and maybe hope for the best?
      There is simply too much to learn and talk about, i wonder if this would be a good way to deal with it.
      So many treatments have been tried over and over, sometimes they work, sometimes they don’t.
      SO that must mean that something was different. This would make it almost mandatory to check what is “wrong” and fix it but every person is special so every treatment must be special for that special person.
      If this is something you already know, i am sorry for wasting time.

      Let me know,

      1. It’s definitely a challenge. Takes a lot of trial and error to figure out. My blood tests in general haven’t shown anything abnormal. Everything from Albumin, to liver function, to glucose, to LDH, to calcium, to tumour markers is within a completely normal range. So I haven’t really learned too much from my bloods.

        1. Very interesting Meech, did you check hormones and immune system? If yes and if they are fine.
          I wonder, since you say the tumor markers are within normal values, did you also get a scan done recently?
          It just sounds like you’re all good now. I hope so.

          Thank You,

          1. Hi Alex,

            Thank you for the concern, it’s appreciated. I actually haven’t checked hormones and I’m not sure which bloods check the immune system but if you mean WBC/neutrophils, etc. Those are all fine too. Unfortunately, the scans aren’t as positive as the bloodwork would suggest.

            1. I would check hormones, glands…..
              PS, stay away from stress!!!

              I find that my mother’s treatment is useless when she is stressed.
              When she is stressed, depressed, pain comes, body odor comes, everything bad comes.


            2. That’s another piece of advice I’d give to those that are healthy 🙂

              I’m working on going back to university and completing a second degree, but in between that I make sure to make time to get down to the lake to walk around, or play guitar, or meditate, etc.

              Like Daniel advises, part of all of this has to be enjoying the day.

      2. Interesting point Alex. It may be the case that ignorant people may live longer.
        And that may be related to their believe and expectation, that someone will take care of them and finally they will be fine.
        Personally, I strongly believe that our desire, believe and expectation has a strong impact on our outcome.
        As a result, use what was successful for others and understand why it will work in your case, do your best, and knowing you did your best expect the best whatever that will be.

        Kind regards,

  3. in a somehow related note to what you guys are discussing here, has any of you read on the story of Krebiozen, a chemo agent developed in the 50s? a doctor, named klopfer injected the then, experimental drug, Krebiozen to one of his very ill patients know as Mr. Wright who seriously believed it was his miracle cure. mr Wright went into complete remission and his disease relapsed only after it turned out Krebiozen was completely ineffective and a total waste of time. very interesting story.

    1. Thank you for that pouya.
      After all the reading i notice a connection between cancer and mood, some sort of hormonal, electrical phenomenon going on.
      Should that be better understood, i feel we would all have something to benefit from.
      I know people in person who have done almost nothing or very little, and they are all fine.
      So far i know of only one certain “cure”. Human teleportation + medical filter enabled. – The computer would filter the bad stuff.
      But yes i know it’s sci-fi. Sorry.
      Meanwhile i think its important to sit back, relax and remember to to tell our loved ones how much we love them.
      Enjoy a nice dinner and some music.
      We all need all the energy we can get, sometimes we need to conserve it. Heal the mind and hope for the rest to work just as well.

      Best wishes,

    2. I did not know that Pouya. It is interesting indeed. I actually very much agree with Alex’s response from above.

      The most important fact beyond all the treatments and chemicals we use seems to be our mind. I was also speaking with someone who worked for an oncology department. He saw constantly that the people who were most positive always lived longer compared to those negative. This is fact. I would actually have much more to say on this line but I save this discussion for when we meet and drink a bier with all the friends from this website – not necessarily all at the same time 🙂

      What is clear to me is that human mind is amazing and science only understand very very little regarding how the human mind works, how the body works and how everything around us works. And btw, I am a scientist at my origin 🙂

      1. Dear Daniel,

        I feel that if we had a good understanding of the mind, brain, organic elements in the body.
        We could then use the machine to induce certain artificial emotions, feelings, signals to the brain.
        This could in theory (according to my understanding of the entire thing so far) bring about a constant fast and certain remission.
        Very few or no chemicals needed. Maybe some higher food intake and with more fruit/vegetables. I’m sure you understand.
        If they can transplant the memories of experienced pilots to non-pilots and have them know the same things in an instant.
        Why would we not be able to transplant health signals to those who are dying.
        While i know this is beyond anything that is being done today, still i felt i had to say it.
        Technology seems to do a lot with war and then some more with – smartphones / planned obsolescence $$$
        We are fitting more and more transistors inside the surface of a red blood cell. Plenty of individual pixels… for that perfect selfie, we’ll do the impossible in that direction…. That’s why we got CERN – Better smartphones, more $. quantum bby.
        Pity we value $ more than people and life.
        While i love technology, the progress made, i can’t help but open my eyes and see how little is being made to make life better.
        There is no CT scanner in my area for example…. and getting one done takes months, paying for it is the full minimum wage.
        If anything comes into making life a little better, it’s expensive, and it’s just an accident it has that usefulness.
        Ex: Thermal Imaging, used for medicine today, in some parts of the world. First use? Kill people. Pathetic….

        Sorry for making it long.
        Have a great time there,

  4. Hi Daniel & All,

    This discussion reminded me of checking out endorphin’s role in regulating cancer & the immune system and found this article: It says 60% of cancer patients can benefit from LDN! Something to consider.

    “The mechanisms involved in the apparent beneficial effect of LDN on cancer have three main elements. The first is the effect of LDN, when taken late at night, in inducing a sharp increase in pituitary and adrenal production of beta-endorphin and metenkephalin, respectively, in the pre-dawn hours, when 90% of the day’s manufacture of these hormones occurs. Most studies have shown that naltrexone induces a two to three-fold increase in production of metenkephalin, the endorphin that most specifically activates delta-opioid receptors, the primary endorphin-related anti-growth factor on cancer cells. The low dose of naltrexone, which in higher doses would block endorphin and enkephalin action on the receptor, is gone from the body in about three or four hours — whereas the elevated levels of endorphins and enkephalins persist all day.

    The second step involved in the anti-cancer effect of these hormones results from direct activation of opioid receptors of cancer cells by the increased endorphins. If this activation occurs while the cell is dividing, it dies. In fact, relatively small concentrations of metenkephalin, when added to human pancreatic cancer cells or human colon cancer cells growing in the test tube, have been shown to kill both. The apparent mechanism of cell killing is called apoptosis (programmed cell death). This appears to be one of the mechanisms by which endorphins and enkephalins combat cancer.

    A third element, which may play a major role in controlling cancer, involves the cells of the immune system, which is regulated/orchestrated to a great extent by endorphins. In particular, endorphins raise the circulating levels of natural killer cells and lymphocyte-activated CD-8 cells, the two immunological cell types that prevent cancer by killing cancer cells as they arise.”

    Endorphin causes cancer cells to die by binding to and activating of the opioid receptors on the surface of the cancer cells. This might explain also how the placebo effect can have such a mighty effect on the patient.

      1. Hi Daniel,

        do you think the CBD works similarly? It could explain why THC content makes it more effective. Whatever makes the mind happy, is good for the body, too?


        1. Hi Helga, with that logic wouldn’t Serotonin be also beneficial to fight cancer? it seems not to be the case.
          if that was the case, I would prescribe Psilocybin for cancer patients. 🙂

          1. Hi Pouya,

            very good point. I was thinking about it a lot. It seems that endorphin is good, serotonin is bad for cancer. They do not have the same effect on the psyche, although it would be difficult for a layperson to tell the difference in the feeling caused by the two molecules. Also, serotonin is a small molecule and neurotransmitter while endorphin is a peptide. I read somewhere that they can antagonize each other but can’t find the reference now. Here is an article about the 4 happiness molecules:

        2. i think so,….. and all the other pain killers that have anti-cancer properties.
          perhaps extasy would be a good one to test?!
          Good solution, Rave+E’s Party the cancer to death.
          Germany has some of the biggest raves, we should all take Daniel to a party and get treatment that way 🙂 *i know a few spots*

        3. Alcohol, heroin, cocaine, and virtually all psychoactive drugs would be very beneficial in the treatment of cancer if this were the case.

          I’d say go out and enjoy life but let’s not jump into scientific reasons for condoning drug use or hedonism. I think it’s fairly obvious that a life of excess is extremely good for your endorphins but horrible for your health.

          1. I would distinguish between drug use for hedonistic purposes and to treat cancer. If you treat your cancer and get ‘high’ as a side effect so be it, no? Of course most drug use is detrimental for health because of addiction. However, taking it in a controlled environment could benefit cancer patients, I’d think.

            1. In this case, the treatment and side effect would be one in the same, no? If I understood you correctly, the euphoria from the drugs would be the treatment. In a sense, getting high to treat cancer. I think it’s a very dangerous proposition and likely not an effective one when we look at things like overeating or drunkenness, which stimulate endorphins. A strong example of how ineffective this would be is the large amount of cancer patients who are on endorphin-stimulating opiates (painkillers) but who don’t see an anti cancer response from this.

            2. Of course I don’t mean an excessive overuse/abuse of drugs. I don’t propose that in any way! Nor am I a drug user, nor have ever been. You are right, opioids for cancer patients don’t seem to solve their cancer. Please, don’t read something into my emails I am clearly not proposing. However, I quite like LDN as it seems to be working well. It also got me thinking what Daniel said about CBD, namely that the variant that has higher THC content works better. Now, would you reject it because it might cause the patient some high?

              There are many things that are beneficial in small/proper amounts but would be detrimental when consumed in excess. Even aloe vera, which clearly has anti-cancer benefits caused rats cancer when used in excessive amounts. I don’t recommend overeating, drunkenness, illicit drug use. If it was not clear to you till now I declare it unambiguously here for your and others’ benefit.

            3. Sorry if I came off aggressively. FWIW I think it’s important to get out and do enjoyable things for both spiritual and physical health. I don’t know if I can quantify the benefit with hormones or cellular microbiology nor if the benefit is quantifiable, but I do strongly believe that these “highs” should be natural – so I apologize if I misread into your comment.

            4. OK, no problem 🙂 Cancer patients are so downbeat most of the time, not the least because of the prognosis their doctor sometimes heartlessly delivers them that some natural or chemically induced relief is highly welcome in most cases. My father was told by his surgeon after removing his colon tumor that he has only x months to live unless he takes chemotherapy. He lived only 9 months anyway. The last chemo (sorry, I have no recollection what it was but it was 14 years ago) that his oncologist got him (and it took her considerable effort to be able to prescribe it for him because of the cost) killed him within 10 days (he just wasted away from it). It is not to say that chemo, especially the modern chemos and the smart strategies Daniel is researching and many others here use cleverly by alternating them with natural treatments and repurposed medications don’t have beneficial effect but it was a bitter and painful experience for us. I would much rather be high than low (within reason, of course).

            5. Dear Helga,
              I am very much impressed by the conversation above.
              CBD oil clearly helped mother but the one we had had almost no THC.
              I’m very strong about diclofenac, she took it in the past in high doses to relief pain, i feel it helped prevent mets and maybe keep the tumor smaller than it would have been.
              If i were to choose death and getting high as a treatment, i’d choose getting high and staying that way if needed for however long needed.
              These political restrictions about cannabis i think they are very much not needed.
              It’s like….. any other thing that is being sold, people get it anyway if that’s what they look for.
              One way or another they will get it, if i was making decisions, i’d make it legal everywhere. Just like all the other things, especially for medical application.
              And if people use it wrong…. their choice. I don’t think we should ban kitchen knifes just because they can hurt someone.
              Anyway, pondering LDN, CBD Oil again, still i feel i should wait for tests and results, then figure out treatment.
              I’m scared to order anything at this point, don’t wish to waste away money on things that may not be needed or actually make my mother’s situation worse even if in theory they help.
              Thanks to Daniel, the foundation, the community and donations, we now feel we have a fighting chance.

              Also i wish to say i am very sorry for your terrible loss. It seems clear that chemo is not the solution people are being promissed, nor are the other 2 options.
              I feel that had we continued with the planned “treatment” my mother wouldn’t have been here with me now.
              So here i come back with. what you said about alternative treatments not being beneficial.
              “Whatever doesn’t kill you, makes you stronger” and i believe that is the case for these alternatives, even if they are ineffective, there is still that placebo….. 😉
              This brings me to citric acid… i understand there is great science behind it, but i don’t see it’s effects on my mother sadly.
              She reports her hair is falling faster with citric acid.

              Many thanks for your continuous presence and help.

  5. What I find incredible is the fact that this LDN was discovered 32 years ago. Still, doctors, oncologists don’t know about it and want nothing to do with it. When I asked a doctor friend if he could prescribe it for me (I thought I had colon cancer), he said, it could be prescribed only by a psychiatrist and only for alcoholics who want to give up drinking. It was at least my experience. Other countries may have less restrictive practices. (Same with cimetidine, it seems.)

    1. i ordered naltrexone (revia i guess) from the philippines. it was cheap (around 40 usd for 10*50mg which will be enough for a year) and the guy is reliable according to many sources. its not low dose, so i need to powder it, put in water and only a drink one tenth of it.

      1. Hmmm … in this case you will need a very sensitive scale to split that in 4.5mg doses …. which is not the case for the cheap digital scales available on the web. Or maybe you already have a solution to that?

    1. Good point Alternmed. That is the approach I used for Salinomycin as very low dose had to be used. The good aspect is that it seems to be soluble in water. I guess the stability is fine.
      Btw, you are exploring many treatment options. What are your findings? Do you see anything that is effective for your case out of what you already tried?

      1. hi alternmed, Daniel
        exactly, the seller was proposing this workaround and to me it seemed OK so i ordered the normal tabs not LDN. im glad you both seem to agree its viable. I have read it works well with HCA and ALA combo and from what i understand it should not interfere with other supplements or drugs.
        Also, to be honest i do not mind extra endorphins.

        1. it arrived today so the seller is reliable if anyone interested. 10 * 50mg tabs, normal naltrexone, it was around 40 usd inc shipping if i remember well. origin was thailand, i misremembered.

        1. Hi Alex,
          Yes, thank you for asking. I am now actually visiting Romania so that I can be next to my wife, since soon it will be her birthday – due to traveling I will be slower in reactions.
          Kind regards,

      1. Dear Daniel,

        Thank you very much for your quick reply.
        i am doing my best and i know it’s not sufficient but that’s all i got.
        I am trying to find out if those things are ok to add.
        Other than that, i am clueless
        Like a caveman in front of a computer….. i try…. if i’m bad at this it must be because i never had to deal with all this before, i don’t know much about medicine/cancer and because those who are meant to know all about this problem we got seem to know very little, at least in my area.
        So i try….
        Then there’s the fear factor…. what if i am doing something stupid.?! And since there’s little EXACT indication of right or wrong…. chances are i’m going to do mistakes, just like before.
        So i don’t know what solutions are serious and what solutions aren’t. What will work and what won’t.
        I am hurting my brain with trying to understand all this, to make the most out of it, logic and reasoning.
        Thank you very much for all the help.
        As you know it means a lot to me and my mother and we wish you all the best, always.
        We pray and think about you, your wife, our friends here. We talk…

        I hope you’ll have a wonderful night.

        1. Hi Alex,

          Statins will lower your LDL levels; however may increase HDL levels.

          Daniel did include a reference saying that HDL increase may actually benefit lung cancer patients.

          If you do opt for statins, lipophilic ones seem to be the more beneficial ones in cancer (I’m sure Daniel covered it in the article). Some of these may include Simvastatin, Atorvastatin, and Lovastatin.

          They’re very easy to get in the Balkans AFAIK.

            1. I’m good man. Same old. I’ll probably be starting on carboplatin soon and hopefully adding diclofenac, DCA, metformin, Simvastatin, dipyridamole, and chloroquine and maybe an intermittent PPI.

              Of course this is all contingent on my kidney and liver cooperating.

              Hope you and your mom are well too.

  6. I think the METABLOC (HCA + ALA) plus Tocotrienols and Coffee (Caffeine) will be a good idea.

    Rosuvastatin Increases Extracellular Adenosine Formation in Humans In Vivo.

    Caffeine promotes anti-tumor immune response during tumor initiation: Involvement of the adenosine A2A receptor.

    Coffee and cancer risk: A meta-analysis of prospective observational studies.

    Targeting the hypoxia-adenosinergic signaling pathway to improve the adoptive immunotherapy of cancer.

    Low, but not high, dose caffeine is a readily available probe for adenosine actions.

    Actions of Caffeine in the Brain with Special Reference to Factors That Contribute to Its Widespread Use.

    1. Indeed, based on the above, Coffee could be a good idea in order to increase the immune system action, via reduction of Tregs. Interesting to know that coffee can impact Tregs via action on A2A receptors, i.e. its inhibition. But next to this we may need stronger metabolic inhibitors or include the pH therapy, to reduce the extracellular protons so that the immune cells can become active. Also, the risk with coffee would be that by inhibiting Tregs, inflammation may occur in advanced cancers. Like one of the ref above is suggesting Caffeine may be best during tumor initiation. I now realize that based on the above, coffee should be avoided by those experiencing auto immune disease.

      1. High consumption of coffee is associated with decreased multiple sclerosis risk; results from two independent studies.

        Coffee consumption and the risk of latent autoimmune diabetes in adults–results from a Swedish case-control study.

        Coffee or tea consumption and the risk of rheumatoid arthritis: a meta-analysis.

    1. Yes, very much agree with Wondering. Awesome links, that connect metabolic treatments with the immune system.
      This is a perspective that place the metabolic treatments as supportive strategies for the activation of immune reactions.

    2. Dear Frank,
      Thank you very much for the valuable links.
      As we see in phlorizin patent,patients are fasting for 8-12 hours+phlorizin to deplete full glucose so deplete the energy of cancer cells.
      But in some of his patients 8-12 hours is not enough so they give phlorizin for 24 hours.
      And the phlorizin+fasting extending the next day after chemo.
      So fasting is a very good idea before chemo but may be not enough.But i am sure it helps.
      Before last chemo we did fasting for 16 hours.
      Kind Regards

  7. see? i connected the dots all alone
    Diclofenac, B1…. i swear i dint read here 🙂
    I’m such a genius 🙂 LOL
    Obviously a lot more to learn……. But i feel proud, good reasons for that. Still i should have payed more attention.
    I find it funny how i decided to alternate aspirin with diclofenac and was asking about b1 the other day
    It’s funny how i find metformin+aspirin to be so good for my mother.
    That moment when you realize you’re too stupid to know you’re a small genius 🙂 Or too scared to see it.
    Too many coincidences no paper and in my mind. You just need the right hints, help, time for that “Aha” moment.
    I hope in the future, not only to have my mother feeling better than ever but to also conclude that the actual root reason cancer is still killing so many is corruption in this day and age and then a small absence of information.
    Feeling positive. 🙂

    Thank you very much for everything, all this help has been overwhelming and we hope it will show positive results.
    Best wishes,

  8. In context of reducing cholesterol.
    What about salt? I find his claims very interesting, but are they something scientifically valid?
    I’m finding i know very little about the cancerous cell, diagram wise, i look at it and i can’t make it out. Idk….. so confusing.
    Thank you very much.

      1. Thank you very much for your reply.
        What salt? I guess the pink salt will be good….. if not please do tell.
        I’m more concerned about the question, to salt or not to salt 🙂 Yes, is salt a good idea or not when trying to reduce cholesterol?
        Some people interviewed like that person, in TY Bollinger’s series “the quest for the cures”, claim that raw salt will not raise cholesterol but the bleached table salt we all consume does due to the processing methods used and additives.
        I fear this may once more be the case of public misinformation the kind where you take honey+ginger to cure cancer 🙂
        So i felt the need to address this concern about SALT, some say it should be lowered, others say it should be increased, then the others who say all you need to do is change the source, after all that being said… the average person would not know what to believe anymore. Especially with sodium levels being within the normal range as it is the case with my mother.

        Thank you so much for everything.

      2. Also dear Daniel,
        Would you agree with simvastatin in being the best choice for inhibition of the mevalonate pathway in NSCLC?
        I’ve read the above but i’m uncertain if that is the best one to go for or not.

        Thank you very much.

  9. Statins dramatically enhance the anti-tumor effects of ACLY inhibition.

    The reduced concentration of citrate in cancer cells: An indicator of cancer aggressiveness and a possible therapeutic target.

    1. Thank you! Great reference supporting the strategy above!
      It looks like sometimes we the need the lab studies to know what the outcome is. Just connecting the research of others may be good enough since we already guessed that the combo of HCA + Statin would be good prior to knowing this reference.

  10. Attention, l’arginine est bonne pour le corps en général car elle dilate les artères et artérioles, comme le viagra, donc permet une meilleur oxygénation et alimentation des cellules. D’où son utilisation par les sportifs.
    Par contre c’est un carburant pour beaucoup de type de cellules cancéreuses.
    Par exemple pour les cancers du sein et de la prostate c’est la privation d’apport externe de l’arginine qui agit contre les cellules cancéreuses comme le montre beaucoups d’études recentes :

    1. Thank you Malypaet. To my knowledge, there is a huge amount of research pointing the towards the positive contribution of statins in cancer, as anti-cancer drugs. Like in any field of science, there will always be someone pointing to the opposite direction. So far I did not came across much science to support its negatives to make me worried.

      1. the frustrating thing is that things like this also depend on the cancer type… we can say metabolism is similar in every cancer…but for treatment there are sooo many things to consider.

        1. Yes W, many may depending on cancer type, and we always need to have an eye on that, but we also need to learn where to draw the line and decide as the world is full of various opinions. Next to that I was looking at the study cited above and its references, and it is not convincing at all to me. One of the points against statins seem to be their impact on Tregs. Actually I was looking a few days ago at that mechanism as Tregs modulation may be also relevant in auto immune disease. Due to exactly this reason, statins were tested on humans with Vitiligo with the hope that there will be an activation of Tregs while on statins and with that stop Vitiligo development. The outcome was that there was no impact on Vitiligo, and that means the immune system activation was not suppressed as intended by statins. This indicates that there may be little to no impact of Statins on Tregs (fortunately for some diseases like cancer and unfortunately for others like auto immune).
          There is so much literature pointing to the value of statins in cancer that I would not worry about its value. But I would check the literature anyway to see what to expect for each cancer. That is what I would do with any new treatment anyway.
          Finally, to me, Statins are an essential piece of the puzzle in the strategy above.

          1. Dear Daniel
            Today i have told my mother to stop taking Mebendazole.
            I have a feeling that it may be the one to blame for the immune system drop
            The tests are available for viewing by anyone here!AgyLnvi3scoTojUrZihYZ4-NM1Ke
            In the table, “inainte de operatie” means before surgery, the others are after that.
            Opinions are welcomed, sorry for the Romanian language there.
            Many many thanks,

          2. Forgot to ask Daniel,
            Would you agree with Simvastatin as being a good choice for NSCLC?
            I read and that seemed to me to be the right one to go for according to theory.

            1. Can you please share the references with us here, Alex? I mean the results of your research trying to find what is most suitable for NSCLC. Thank you.

            2. Titles sound encouraging, the contents are mostly beyond me, that’s why i ask here.
              I appreciate your attempts to help me in understanding it all for myself, still i find myself reading things like that and at the end of the night i realize i understand nothing.
              The priest baptizing me said i’d be a philosopher 😀 – true story.
              To me it sounded like Simvastatin would be the one to go for, but as with anything in this adventure, i’m not sure it makes the best sense based on the information out there that i can’t understand most of the time.
              Thank you so much for everything.

            3. Thank you so much Daniel for your priceless help.
              it is sad that my mom felt very sick when she did take a single pill of itraconazole.
              I am however wondering if GcMAF, Avemar, CBD Oil, LDN, Germanium. Apigenin could work with DCA in your experience or opinion based on all the theory behind cancer and your extensive research.
              Thank you very much.

          3. On top of this I’d like to add that there’s a world of difference between “cancer causing” and “cancer fuelling”.

            Most chemotherapies are carcinogenic in that they can cause secondary malignancy, but they’re also extremely anti-proliferative in that they impede tumour cells from spreading or growing, and kill them in most cases.

            I’d argue that a lot of treatments (if not most) have the potential to be carcinogenic as they’ll alter the way at least some healthy cells function, which can lead to malignancy. The risk is undoubtedly pretty low.

            Non-toxic avenues to destroying cancer cells seem like a bit of a pipe dream to me at this point. Cancer cells utilize pathways that normal cells utilize, and therefore there will always be some collateral damage, and some potential to do harm to yourself. It’s just about balancing those risks with the risks the cancer itself poses and determining which risks are worth taking.

            Just my two cents.

            1. Meech, you are so young and so sharp. You expressed perfectly what I wanted to write last evening, and better than I would do. I actually wanted to write about the difference between “cancer prevention” and “advanced cancer fighting”, but then I thought it may be unfair for Statin since it has been shown in many studies that helps prevent or reduce the spread of cancer vs. those patients not using Statins.

            2. Yes, cancer patients dont care about etoposide induced leukemia in 20 years. Im in for that! 🙂

              By the way, i fully agree.

  11. Coinhibition of ACLY and ACSS2 caused a dramatic increase in the number of cells in early-apoptotic cell fraction.
    It shows that coinhibition of the 2 pathways known to be involved in cytosolic acetyl-CoA production in cancer cells is highly cytotoxic for the cells.

    1. Thanks Frank. Indeed, this combination should work nicely. For ACSS2 inhibition I would use multiple strategies just to make sure we incraese the chance of achieving that. That means I would use all we discussed, i.e. Vitamin E, Apigenin, and possibly proton pumps inhibitors. MCT1 inhibitors will lower the amount of Acetate absorbed just in case we do not inhibit ACSS2 and Stains will inhibit mevalonate pathway just in case ACLY was not well inhibited. Using two inhibitors for each target will increase the chance for doing the job. Do you know any other accessible ACLY inhibitor, other than HCA?

  12. I’m starting today with:

    1500mg Metformin
    20mg Simvastatin
    375mg Dipyridamole
    1500mg HCA
    400mg Chloroquine
    32mg/kg DCA

    Along with some natural supplements (milk thistle, propolis, curcumin, EGCG)

    I have diclofenac but I accidentally ripped out my nephrostomy tube from my kidney last night and had to get it replaced so I’m having bleeding due to that and would like to let it heal. I’ve been taking 50mg of it lately but think I should probably increase it. I will probably start carboplatin at an adjusted schedule with Mesna injections with Dr. Khan next week (called SEF chemo). I went and spoke to four patients who were doing this chemo – one ovarian, one melanoma, one prostate, and one breast; all of whom were having a good response to the therapy.

    Any thoughts? Daniel/others? I know with chloroquine, I will probably have to include a PPI as well, so I haven’t taken the chloroquine yet, as I don’t have a PPI on me at the moment.

  13. I wrote a comment and it looks like it didn’t post, I’ll try re-writing it.

    I’m starting today on:

    1500mg Metformin
    32mg/kg DCA
    20mg Simvastatin
    375mg Dipyridamole
    1500mg HCA
    400mg Chloroquine (Possibly. Since I don’t have a PPI at the moment, I don’t know if it’s worth it to “waste” pills that may not enter the tumour)

    I have diclofenac but I accidentally ripped my nephrostomy tube out of my kidney last night and had to have it replaced, which has caused bleeding and I think it may be best to let the wounds recover before taking this one.

    I’ll also be adding the parsley Daniel recommended.

    I’m also starting SEF Chemo next week at Medicor. I spoke to a few patients who are all having good responses to it. The base chemo is carboplatin, with an adjusted dosing schedule, and a “cell protecting” agent called Mesna, which is supposed to keep your blood counts from dropping. The patients I talked to had mostly normal blood counts but sustained response.

    Any thoughts? Things I should add/remove/look to alter slightly?

    Thanks everyone.

      1. Hi Meech,

        It is difficult for me to tolerate 100 mg of dipyridamole. For the next hour I feel very tired and with muscle aches all over. I take it before going to sleep and early in the morning. I cannot imaging taking more than 200mg…

    1. Hi Meech,

      Thank you for your update. I am sorry to hear bout the tube.
      Answering a former question: combining Oxaliplatin/Ciplatin with Omeprazole, I would do that only if there is no response without.
      Regarding the above:
      – I would not add multiple new elements at the same time
      – I would add Piperine supplements – very important I think
      – I would check the interaction of Mesna with the old and new drugs added
      – Dipyridamole is also adding to the bleeding risks for the current situation

      Kind regards,

      1. – Makes sense on combining a PPI with a platin. I agree. Would you then not do the chloroquine + platin or would you do it anyway despite possible difficulty getting to the tumour. It seems fairly valuable when combined with chemo.

        – I’ll look into piperine. Should be easy to find. I think my curcumin supplement also comes with piperine.

        – I’ve decided to titrate the diclofenac for the particular reason of bleeding (and the side effects). So I’m starting with 150mg/day for the first bit until I get used to it.

        – I’ll check the Mesna.

        Thanks for the advice!

        1. Hi Meech,
          If i were you,i would use nothing before or with chemo in the first 3 course.
          Than add 1 by 1 if no responce.
          Thats my thought.
          Kind Regards

          1. Hi Ergin,

            Thanks for the advice. The only thing is that I’m paying a good amount of money per cycle of this chemo and so I’m not sure how many cycles I will have but I am definitely thinking of taking that approach.

            Why, in particular, would you advise this? Have you had to make a similar decision?

            1. I think Ergin gave a good piece of advice here.

              You never know what side effects you can develop from taking chemo with other medications. Low dose metformin (125mg daily!) caused me severe proctitis like symptoms while I was on chemo. I had to stop and restart metformin a few times before I figured out the cause. Otherwise the symptoms could be mistaken for just another side effect of chemo. This combination made my chemo almost intolerable.

              I am taking metformin after chemo with no problem.

            2. Thank you Tanya for the advice and sharing your experience. It is very valuable and I am definitely reconsidering my options.

          2. After i saw the big reaction with chemo,i was thinking every posibilities.
            Which one?Chloroquine,itracanazole,diclofenac,mebendazole?
            I hope you understand what i mean.I am not talking on effectiveness.
            Now i cant give any of them,because i will never know which one made reaction.
            So we cant give plaxitaxel also.

            1. Absolutely Ergin, thank you for the advice. I had actually not envisioned that problem. It’s definitely something to think over but I am reconsidering the approach now.

        2. Hi Meech,

          The comments of Ergin and Tanya are very valuable. There is a chance for interaction and side effects that may affect your core treatment (Mesna + platin). So starting on the low side with additions may be wise. We will off course never know in advance what is best in practice but at least verify well each of the drugs you decide to use. In the end, this is not first time for you having chemo? And you know yourself best. Piperine makes sense from the point of view of the strategy mentioned in the post above. Because it may also have anti oxidant properties, I would use it latter when off chemo.

          1. Thanks Daniel. I have actually contacted some doctors familiar with drug repurposing and will hopefully see with them the type of experiences they’ve had, etc. For now, I am stopping the medication for the short term and resuming with my normal DCA/Metformin focused approach.

            1. Dear Meech,
              First of all, i want to wish you good luck with whatever you choose. I think the randomness of things is something we can pray for to be on the positive side and not on the negative side. In the end everything is to some degree random.
              Indeed we can do our best to try to have things go on a specific path but luck is needed. 🙂 So i hope you get plenty of it
              I am guessing you didn’t see any signs of stability or reversal of disease with DCA, Metformin combo or alone, so you now want to combine them with the standard treatments.
              Or have you?
              I wish i could do more for you and everyone else here and not just here. I wish i could help everyone not just mother.
              Still uncertain if i will even succeed with my mom. Hence i ask if DCA helped you considerably and if so in what way.
              My mother’s bump on the left arm that is changing fullness and a bit of size for months is now flat and “lifeless”, a normalization. It’s been a week since we started DCA 2000mg / day orally.
              If it’s not a tumor, what would be desired? For it to get larger and fuller or smaller to nothing?
              Any opinion, experience, is most welcomed. So i ask anyone taking DCA or who has taken DCA if they had ANY change, good or bad.
              Thank you so much, and Good Luck !!!

            2. All day i feel sorry if i gave you a negative energy or not.It is a big responsibilty for me,more than that i can lift.
              But Meech,you know the reason.We are nearly using the same drugs.
              Good luck brother.

            3. Me? Negative energy from you? I am full… no more negative can fit in me. From now only positive energy 🙂
              I accept what the universe has to offer to me, i am ready for it’s random changes 🙂 Good or bad, it’s the nature of the universe and life, me, my mother, you everyone. We are all part of it.
              I accept what it will do, good or bad. I will only attempt to make it less random, just a little, and i can only hope that will be enough to prevent the ultimate inevitable death of my mother. As we all die but live as if we are immortals.
              I looked into my eyes using a mirror today, as i have not done so in a long time. I saw signs of liver damage.
              I learned a lot during these months, enough to see problems of health where doctors wouldn’t be able to tell if they are normal or not. At least the doctors here around me.
              In the end i will try to do my best to help as much as i can and maybe improve my health in the process.
              So i ask if you do DCA now? Did you see any results from DCA? I am considering Closer regulation of my mother’s diet to the Restricted Ketogenic Diet, sounds like it could help a bit.
              I keep wondering if immune boosting supliments are key in healing from this.
              Like… what if? What if the immune system was running at FULL CAPPACITY? What if we would then help it with a little bit of this and a little bit of that? I wonder if we would have more chances.
              I wish you good luck too bro,

            4. Hi Alex,
              I am really sorry that you catch me at night and friday night.
              My thoughts are very different about acids.Any name that has acid at the end.
              If i would be the patient,i would never use acids oral.Only iv.
              Sorry Alex, iam not an expert nor a doctor nor a scientist.Just small experiments and a flow chart.
              And you know how i am interested in blood counts.
              Especially LDH.
              Kind Regards

            5. but acids are everywhere in nature and in the body bro sometimes acids are good, think about gastric acid 🙂

            6. Hi Alex,

              I can’t say that Metformin and DCA and Keto haven’t helped. I was given a horrible prognosis of 8-12 months and have survived for over 36 months now and am in fairly good shape, and able to play sports, etc. I have had no conventional systemic treatment since June of 2015.

              My tumour Ki-67% score was 80%. If you’re unsure, Ki-67 is a protein expressed by all cells in a sample which are dividing; which means that 80% of my tumour’s cells are supposed to be dividing at any given time. A low grade tumour (for my type) is under 1%, a medium grade tumour is up to 25%, and anything above 25% is considered high grade.

              So for me to say that they haven’t helped would be hard. They may have very well slowed the growth but they haven’t stopped proliferation or growth. I have probably 15 tumours + inummerable lung nodules in all six lobes. So now is the time to try to eliminate some for at least a period of time before maybe trying to go for the less-toxic approaches for maintenance.

              I hope this helps.

            7. Thank you Meech for that valuable reply. I appreciate it.
              I wonder what are your latest immune cell counts? I’m trying to see if a beefy immune system is able to get rid of the cancer. SO if the case would be that you have your immune system at full capacity, given that you still have disease progression, it would “prove” that boosting the immune system is not the solution to end all problems.
              What about DCA and Metformin? Have you been taking them on and off or continuously?

              Many many thanks,

            8. My blood cell counts in general over the past 2.5 years have been stellar with no complaints so I’d assume the immune ones are too.

              I don’t think it’s a defect of the immune system that it isn’t killing the cancer cells. I think it’s working just as it should given the characteristics that cancer cells possess. The cancer cells are still “us”, and are still expressing natural biomarkers which normal cells express.

              One of the potential side effects of immunotherapy (which tries to get your immune cells to recognize your cancer as foreign) is myesthenia gravis, where the immune system starts to attack muscle cells.

              So in conclusion: I don’t think keeping your immune counts at healthy levels will cause the immune system to attack the cancer. But if you’re using some sort of immune-modulating therapy then it’s probably pretty imperative to keep the blood counts up. And just for general health, it would be important.

            9. Hi Alex,
              Also in InCVAX,they use Low dose cyclophosphamide inorder to deplet Tregs.
              I believe that theory.And you know the rest.Necrosis and releasing enzyemes from dying cancer cells makes immunity to recognize cancer.
              And i dont think that those stage4 patients heavily preatreated with chemo has a perfect immunity.
              Kind Regards

            10. I forgot to thank you and Ergin for the words.

              I’d also like to say that for the sake of the website, I try to keep most of my comments here science or experience based and strictly protocol oriented to help people with the medicinal side of things. However I’m a very religious person and strongly believe that this has been one of the keys to my survival. I 100% agree with Daniel that time needs to be taken to feed the spirituality.

              Good luck to all here.

  14. Thank you again for all the help and these priceless articles.
    I am wondering if i can potentiate DCA’s effect with Vitamin B1
    How can i check if my mother’s cancer is expected to show scavenger receptor class B type 1 (SR-B1) receptor?

    Many thanks,

  15. Sadly my mom had a bad reaction to itraconazole, i was wondering if Ezitimibe could cause the same effect if it’s a similar drug that may work the same.
    THank you

          1. sadly some things are not available here, but whatever is available is usually easy to get, it only takes money.
            I could help if you feel that’s what you need or other drugs but customs, if any. will ask for prescription. Depends…
            Let me know

            1. Marcos, can you send me your email and I will try explaining the various concerns/dosages and the intricacies around the system.

            2. Hi Meech

              I don’t know how to get your email within the forum,if you are able to get the mine please can you send me the information .Thank you for your kindness

  16. Hi, I’m new to this topic “cholesterol and cancer”, and sorry I got this wrong, but wouldn’t it be enough to solely block the MVA pathway? I read that all forms of cholesterol have to go through this pathway to form. I just don’t understand why you need to block the ACLYL in point 3 and than block the MVA pathway in point 4? Statins alone inhibit HMG-CoA and interfere with cell signaling, thus, Statins and Bisphosphonates seem to be enough to get the job done. Is there really a need to take all the supplements and drugs listed above? (Expect for the metformin and the anti-viral/fungal drugs) Thanks in advance.

    1. Hi Katy,

      This is a fair question.

      As discussed in the article above, at any given moment a cell has a few more options to access cholesterol other than producing it via MVA pathway. For example, it can access the cholesterol already previously produced and stored as lipid droplets. But besides MVA, there is another way cancer cell can produce cholesterol with the help of ACSS2 enzyme (see above).
      However, even if MVA would be the only way to obtain Cholesterol (which is not), some drugs can work better for some people and less for others (different absorption and pharmacokinetics). In addition, some drugs can penetrate better better some cancer cells and less good others. In general, non of these drugs will totally inhibit such pathways, but hopefully reduce their activity.

      The expended strategy above is intended to increase the chance for altering cholesterol production in cancer cells by:
      1. addressing different routes through which cholesterol can be made available within the cell
      2. addressing the most important cholesterol producing pathways such as MVA at multiple points
      to finally increase the chance of achieving the goal.

      I hope this clarifies and answers your question.

      Kind regards,

      1. Hi Daniel, thanks for your detailed answer 🙂 Yes, it clarafied my questions. Do you happen to know if it would make sense to use LXR agonists instead of statins and metformin? They are known to inhibit cholesterol trafficking by blocking oncogenic signaling, disrupt glycolysis (Warburg effect) and lipogenesis all at once. SR9243 is known to have these effects, but there are also studies conducted with quercetin and it’s inhibitory effect on mTOR singaling. I would love to hear your toughts on this.

        Thanks in advance.
        – Katy

        1. Hi Katy,

          Thanks a lot for your very helpful question. I did some reading on LXR and I indeed find it as a very relevant “knob” specifically in hormonal cancers. Not only that it can help modulate various cholesterol production/import related mechanisms, but also has impact on inflammation and can affect Steroid synthesis
          Here is a list containing natural LXR agonists
          Of all, the one I prefer is Honokiol due to its multiple anti cancer mechanisms.
          Next to that, according to the elements suggested in the paper, I found this supplement that may be a good one which contains Plant phytosterols including ß-sitosterol, campesterol, stigmasterol, brassicasterol, and sitostanol

          I hope this answers your questions, and I hope you are going to further contribute on this website. 🙂

          Kind regards,

  17. Hi All. A few comments regarding statins:
    1) The anticancer effect of statins may not be from reducing cholesterol, but from inhibiting the production of isoprenoids, which is downstream of HMG CoA reductase, the enzyme that statins inhibit. See:
    2) Isoprenylation of the RAS protein, which is mutated in 75% of pancreatic cancers, may be inhibited by compounds which have terpenes or isoprenoid groups. These include a wide variety of supplements which are known to have anti cancer activity including boswellia, squalene, and tocotrienols (a form of Vitamin E). see: Isoprenylation as an anticancer strategy:
    3) Among all the various terpenoids and isoprenoids that inhibit HMG CoA reductase, the tocotrienols appear to be the most potent:
    4) The tocotrienols, which are a form of Vitamin E appear to be quite safe. Tocotrienols were used in a study with ovarian cancer patients with good results. 300mg 3 times per day was well tolerated:
    5) Statins alone, or isoprenoids alone have modest effect on cancer cells, but the combination of statins plus tocotrienols is extremely potent. See:
    6) To answer Zdenek’s question, there is some evidence that the lipophillic statins: simvastatin, atorvastatin, and lovastatin have better effect in breast cancer than hydrophillic statins (pravastatin, rosuvastatin, and fluvastatin). See:

  18. Hi Daniel,

    We need to adjust our strategies right away as my husband’s tumor marker came back today – his PSA increased 50% in two weeks. He is seriously resistant to ADT – including Xtandi. I would like him to add Atorvastin 20mg a day – we already have the script but he was holding off as he has been ramping up on Metformin, currently at 500 mg daily split between two meals – goal is to take 1 gram daily.

    His cholesterol level was measured this week at 106 (not the complete panel). The only dietary fat is flax oil, occasionally a very little organic olive oil. He is concerned and feels that 106 is possibly low enough. Do you feel adding Atorvastin would safe or would his cholesterol level fall even lower and be too low? He is on the low-dose aspirin daily (which I saw there is a study that combining a statin and aspirin could be more beneficial for prostate cancer). He still has a good appetite and energy level – thanks to Fenbendazole.

    I am also seriously looking at the Vitamin C and Doxycycline protocol. If he is successful currently at starving the cancer of cholesterol, and he is not consuming sugars, dairy, meat (he is quite thin as well) could the timing be now to begin the Doxy, ramp it up and in two weeks or so start the IVC treatments? I would appreciate your thoughts and feedback greatly.

    Thank you,

  19. Dear Daniel
    i came across one article where it is saying that – “Cholesterol inhibits the opening of the mPTP by preventing integration of the pro-apoptotic Bcl-2-associated X protein (BAX) in the outer mitochondrial membrane. This inhibition explains how elevated LDL reduces mitochondrial dysfunction by preventing loss of the active site of oxidative phosphorylation from mitochondria.”

    and another article – “Therefore, activation of mPTP may provide a new strategy to sensitize cancer cells to chemotherapeutic drugs and to reverse the MDR in cancer cells.”

    I have a difficulties in interpretation of these 2 articles. Does these mean we can combine the cholesterol strategy with conventional treatments such as chemotherapy?

    Thank you

    1. Dear Asaf,

      Thank you for your interesting question. I will have to look into the articles you mentioned to understand better what are the statements. But in any case, the anti-cholesterol strategy should work well with chemo.

      Kind regards,

      1. Hi Daniel, this link refers to the chemopreventive (not chemotherapy) action of aspirin + Curcumin + sulforaphane in the case of pancreatic cancer.

        Do you have any thoughts on using the Above combination + Hydroxychloroquine as a Autophagy inhibitor + Mebendazole/Fenbendazole together at the same time as FOLFIRINOX chemotherapy ? Is there any information on the mechanism of folfirinox and therefore if any of the above supplements could be counter-productive to use at the same time as the Folfirinox?

        1. Dear gmt,

          Here you can find the chemos included in the FOLFIRINOX cocktail and you can look at the mechanism related to each of those.

          Below, is the treatment protocol used recently by a patient I am in contact with offline and there was a response to FOLFIRINOX with a large decline in markers. It is not clear if it is because of this supporting therapy, but it is possible this contributed to the good results. I will just paste the info from the document they put together after our discussion.

          I hope it helps!

          Kind regards,

          Chemotherapy (FOLFIRINOX) will start at 25 November 2019

          Metformine, started on: Saturday 9 November 2019
          1) Started with 500 mg until 14 November 2019.
          15 November 2019, started with 1000 mg until 22 November 2019.
          Chemo will start at 25 November 2019, stop using 3 days before chemo.

          2) Second chemo will start on 23 December 2019, stop using 3 days before chemo.
          23 December 2019, start with 1000 mg.

          Mebendazole, started on: Sunday 10 November 2019
          1) Started with 200 mg until 15 November 2019.
          500 mg will be taken from 16 November 2019 until 22 November 2019.
          Chemo will start on 25 November 2019, stop using 3 days before chemo.
          26 November 2019, start again with 200 mg during the chemo.
          28 November 2019, 300 mg
          29 November 2019, 500 mg

          2) Second chemo will start on 23 December 2019, stop 3 days before chemo.
          24 December 2019, start with 200 mg.
          26 November 2019, 300 mg
          27 November 2019, 500 mg

          Milk Thistle, started on: Monday 11 November 2019
          1) Started with 1000 mg, until 24 November 2019.
          Use 500 mg per day during chemotherapy.
          Chemo will start on 25 November 2019, stop using 1 day before chemo.
          30 November 2019, start again with 500 mg and than increase to 1000 mg.

          2) Second chemo will start on 23 November 2019, stop 1 day before chemo with 1000 mg.
          28 December 2019, start with 500 mg than increase to 1000 mg.

          Aspirine, started on: Monday 11 November 2019
          This has been stopped because of the interaction with Citalopram.

          Coriolus, started on: Wednesday 13 November 2019
          Started with 4 pills of 620 mg = total 2480 mg.
          This medication will be continued during chemo with the same dose.

          Melatonine, started on: Wednesday 13 November 2019
          1) Started with 5 mg before bedtime until 16 November 2019 than 20 mg.
          16 November 2019 using 20 mg until 24 November 2019.
          Chemo will start on 25 November 2019, stop this medication on 24 November 2019 than start again on 27/28 November 2019 with 5 ore 10 mg.

          2) Second chemo will start on 23 December 2019, stop 1 day before chemo.
          25/26 December 2019 start with 5 ore 10 mg.

          D3 vitamine, started on: Thursday 14 November 2019
          1) Started with 5000 ui until 19 November 2019.
          19 November increased to 10.000 ui
          Chemo will start on 25 November 2019, stop 1 day before chemo.
          Than start 3 days after the chemo on: 28 November 2019 with 10.000

          2) Second chemo will start on 23 December 2019, stop 1 day before chemo.
          Than start 3 days after the chemo on: 25 December 2019 with 10.000 ui.

          Atorvastatine, started on: Friday 15 November 2019
          1) Started with 40 mg until 20 November 2019.
          Chemo will start at 25 November 2019, stop 3 days before chemo on: 22 November 2019.
          Than start again 1/2 days after the chemo on: 26/27 November 2019 with 40 mg.

          2) Second chemo will start on 23 December 2019, stop 3 day before chemo on: 20 December 2019.
          Than start again 1/2 days after the chemo on: 25/26 December 2019 with 40 mg.

          Curcumin, started on: Wednesday 23 November 2019
          1) Started with 1000mg until 30 October 2019, 1 pill fish oil EPA 600mg and DHA 400mg
          Started with 2000mg until 6 November 2019, 2 pills fish oil “ “ “ “ “
          Started with 6000mg until 15 November 2019, 4 pills fish oil “ “ “ “ “
          Started with 8000mg stop 1 day before chemo on: 24 November 2019.
          Start 5 days after chemo on: 30 November 2019 with 8000 mg and 4 pills fish oil EPA 600mg and DHA 400mg.

          2) Second chemo will start on 23 December 2019, 2 days before chemo on: 21 December 2019 stopped with Curcumin and fish oil. Than 5 days after chemo start again on 28 December 2019 with Curcumin 8000 mg and 400 mg fish oil.

          Doxycycline, started on: Saturday 23 November 2019
          Use this medicine during the chemo 100 mg in the morning and 100 mg in the evening.
          Daniel say: Depending on the results whether this will be contunted.
          Daniel say: break for 1 month, we’ll talk about this later.

          Probiotic, started on: 27 November 2019
          1 time in the morning and 1 time in the evening.

          1. Thank you Daniel.

            1. It seems here that Doxycycline is used as a autophagy inhibitor instead of Hydroxychloroquine. If I understand this correctly, in the case of a autophagy inhibitor, one would want to use it on the same day as the chemotherapy (unlike metformin, Curcumin or other anti-oxidants that would be stopped before the start of chemotherapy). Is my understanding correct that autophagy inhibitor is to be used on the same day as the chemotherapy ?

            2. Is there any difference between the use of Vitamin D orally /intramuscularly or intravenously ?


  20. I came today around article about apigenin – it was glass and mouse tested alone and showed anti-cancer effect on chondrosarcoma cells.
    “Apigenin inhibits proliferation of human chondrosarcoma cells via cell cycle arrest and mitochondrial apoptosis induced by ROS generation-an in vitro and in vivo study”
    2 and 5 mg/kg dose was used.
    According to
    “Fresh parsley leaves (P. crispum) were purchased from a local store (Lodz, Poland) and dried at 150°C for 30 min prior to use.”
    Petroselinum crispum 126 – 137 mg/g

    So, 4g of dried parsley will be enough for 50kg adult.

    If it is pro-oxidant then could it be combined with chemo (if drugs interactions is clear)?

      1. Thank you very much Daniel.

        I use my time now to prepare drug candidate list, so Apigenin is added there along with contact kindly provided by you.

        The previous article described IP administered Apigenin and there is another where daily 300 mg/day oral administration of Apigenin inhibited adenocarcinoma growth (up to noticeable extend):
        Regarding toxicity – on mouse liver toxicity at 100 mg/day for IP admistration on mouse was observed:

        What are usual Apigenin IP administration on humans?

        In case if others are interested in Apigenin content in (possibly wet) parsley – maximum soxhlet ethanol extraction yielded in 1756.36 mg apigenin/100 g parsley:

        It seems that Apigenin also might help to overcome chemo drug resistance:
        “Apigenin reduced the mRNA expression of multidrug resistance 1 (MDR1) and multidrug resistance‑associated proteins (MRPs) in MCF‑7/ADR cells.”

        What a wonderful parsley.

        Kind Regards

  21. @daniel

    Thanks Daniel. Actually I had seen the example of the doctor who used paricalcitol intravenously which is why I was curious. On the Hydroxychloroquine taken orally, the doctor refers to a dosage of 600 ug BID in the attached (third paragraph in background section).

    I am not able to understand what that “600ug BID” dosage means in terms of a oral tablet dosage ? Would it be 200 mg of hydroxychloroquine taken orally or more ? Can you pls. help me understand.


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