Anti Cholesterol Strategy to Fight Cancer

Background

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 http://www.nature.com/nrc/journal/v16/n11/fig_tab/nrc.2016.76_F1.html

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 https://www.cancertreatmentsresearch.com/itraconazole/. 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 https://www.cancertreatmentsresearch.com/bisphosphonates/ 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 stored inside the cell: lipid droplets

As discussed in a previous post as well https://www.cancertreatmentsresearch.com/cholesterol-cancer-acat-inhibition/, 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.

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 https://www.cancertreatmentsresearch.com/acetate-fuels-cancer/ 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 http://cancerres.aacrjournals.org/content/72/15/3709

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 https://www.cancertreatmentsresearch.com/itraconazole/
    • Dose & Source: see my post on Itraconazole at the link above
      .
  3. reduced Citrate conversion into acetyl-CoA that would be otherwise further used on the mevalonate pathway: used HCA supplement to inhibit ACLYL https://www.cancertreatmentsresearch.com/another-weak-spot-of-many-cancer-cells-atp-citrate-lyase-inhibition/
    • 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.
      .
  4. inhibit mevalonate pathway: use Statins and maybe bisphosphonates. Specifically, I would chose a Lipophilic statins as those have been shown to be the most active (see Reference section).
    • Dose: 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.)
      Indeed recent research indicates that “Statin and Bisphosphonate Induce Starvation in Fast-Growing Cancer Cell Lines
      .
  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. So dipyridamole is a must have in order to maintain statins effectiveness (Ref.).
    • Dose: 200mg 2 x day
    • Source: any pharmacy
      Note: Thank you to Frank Liu for heads up on this point via his comment.
      .
  6. inhibit storage of cholesterol as lipid droplets: use ACAT1 inhibitors such as Piperine supplements (Ref.)
    • Dose & Source: see my post on ACAT inhibitors at the link above
      .
  7. reduce the import of acetate and ketone bodies by inhibiting MCT1 with NSAIDs such as Diclofenac, as discussed here https://www.cancertreatmentsresearch.com/ph-cancer-a-top-treatment-strategy/#comment-2838
    • Dose: see the link above indicating typical dose used to inhibit MCT1
    • Source: any pharmacy as capsules, suppository or topical application
      .
  8. 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 attenuate 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.
    Interestingly, low extracellular pH also activates SREBP-2. Here is a very recent paper on that https://www.ncbi.nlm.nih.gov/pubmed/28249167 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 https://www.cancertreatmentsresearch.com/ph-cancer-a-top-treatment-strategy/

    • Dose: not yet sure what would be the best dose of tocotrienols – to be determined
    • 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.
      .
  9. Metformin (or Doxycycline) 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 may also have the capability to reduce Mevalonate pathway activity, in a way similar to that of statins (Ref.). Furthermore, Metfomin has been found to reduce LDL levels (Ref.1, Ref.2)
    • Dose: typical Metformin target dose 1000mg to 2000mg/day, starting from 500mg and moving slowly up to the target dose
    • Source: any pharmacy
      .
  10. Another point that could be addressed to further strengthen this strategy is 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 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 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.). Yet, 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.)

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 https://www.cancertreatmentsresearch.com/1443/

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.)

References

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

Additive antitumor effects of celecoxib and simvastatin on head and neck squamous cell carcinoma in vitro https://www.spandidos-publications.com/10.3892/ijo.2017.4071

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.

Disclaimer:

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

Please read an extended version of the Disclaimer here: https://www.cancertreatmentsresearch.com/?page_id=1794

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150 Comments on "Anti Cholesterol Strategy to Fight Cancer"

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Carl
Member

Excellent summary! Thanks Daniel

Ergin
Member

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.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617942/
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
Ergin

Meech
Member

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.

Alex
Member
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… Read more »
Meech
Member

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.

Alex
Member

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,
Alex

Meech
Member

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.

Alex
Member

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.

Cheers.

Meech
Member

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.

Pouya
Member

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.

Alex
Member
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… Read more »
Helga
Member
Hi Daniel & All, This discussion reminded me of checking out endorphin’s role in regulating cancer & the immune system and found this article: http://www.lowdosenaltrexone.org/ldn_and_cancer.htm 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… Read more »
Helga
Member

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.)

Wondering
Guest

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.

alternmed
Member

hi all,

just dissolve the natrexol pill or capsule in 50 ml of water,let it in a fridge and just shake it before taking the 4.5/5 mg/ml of water from it.best before sleeping

alternmed
Member

hi daniel

we are trying pdt right now,i ll need to wait the pet scan before sharing anything .

Alex
Member

B1 to reduce colesterol
Pumpkin seeds and apple cider vinegar for sodium/adrenal glands?

Thank you very much,
Alex

Frank Liu
Guest

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.
http://atvb.ahajournals.org/content/29/6/963.long

Caffeine promotes anti-tumor immune response during tumor initiation: Involvement of the adenosine A2A receptor.
http://www.sciencedirect.com/science/article/pii/S0006295215005377
https://www.researchgate.net/profile/Amos_Douvdevani/publication/281195178_Caffeine_promotes_anti-tumor_immune_response_during_tumor_initiation_Involvement_of_the_adenosine_A2A_receptor/links/560ce0d208ae6c9b0c42db82.pdf?origin=publication_detail

Coffee and cancer risk: A meta-analysis of prospective observational studies.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5036059/

Targeting the hypoxia-adenosinergic signaling pathway to improve the adoptive immunotherapy of cancer.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576025/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576025/figure/F1/

Low, but not high, dose caffeine is a readily available probe for adenosine actions.
http://www.sciencedirect.com/science/article/pii/S0098299716300802

Actions of Caffeine in the Brain with Special Reference to Factors That Contribute to Its Widespread Use.
http://pharmrev.aspetjournals.org/content/51/1/83.long
http://pharmrev.aspetjournals.org/content/pharmrev/51/1/83/F1.large.jpg?width=800&height=600&carousel=1

Frank Liu
Guest
Wondering
Guest

thanks, awesome links!

Ergin
Member

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
Ergin

Alex
Member
see? i connected the dots all alone Diclofenac, B1…. i swear i dint read here 🙂 I’m such a genius 🙂 https://www.youtube.com/watch?v=6gpBvMdrQDc 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… Read more »
Alex
Member

In context of reducing cholesterol.
What about salt? https://youtu.be/3nBH7Crkzxk 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.
Alex

sirsna
Member

Thank You Daniel and Frank Liu for recent updates and links!
Just started to take my dipyridamole, but I take low dose at the first.

ieva

Frank Liu
Guest

Statins dramatically enhance the anti-tumor effects of ACLY inhibition.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3407542/

The reduced concentration of citrate in cancer cells: An indicator of cancer aggressiveness and a possible therapeutic target.
https://www.ncbi.nlm.nih.gov/pubmed/27912843
http://www.journals.elsevierhealth.com/cms/attachment/2082633036/2072860597/gr1_lrg.jpg
http://www.journals.elsevierhealth.com/cms/attachment/2082633036/2072860598/gr2_lrg.jpg

Alex
Member

So what did they use in there?
What worked?
I can’t make out the actual information inside the scientific mambo jambo
interesting….

malypaet
Member

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 :
https://www.researchgate.net/publication/311995057_l-Arginine_Uptake_and_Its_Role_in_the_Survival_of_Breast_Cancer_Cells

malypaet
Member

Take care about statin, a lot of publications show that it increase the risk of cancer:
Sometime positive ans sometime negative:
http://www.healthline.com/health/high-cholesterol/do-statins-cause-cancer

malypaet
Member

Take care also with arginine, it can ne used as fuel for cancer cells (Breast, prostate,…):
https://www.ncbi.nlm.nih.gov/pubmed/24692592
Arginine dilates arteries and arterioles, such as viagra, which allows a better nourishment of cells in oxygen and nutrients, very used by athletes. Near the cancer cells, its effect disappears on arterioles because it is aspirated as fuel by these, like glucose.

Frank Liu
Guest

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.
http://mct.aacrjournals.org/content/11/9/1925.long
http://mct.aacrjournals.org/content/molcanther/11/9/1925/F7.large.jpg
http://mct.aacrjournals.org/content/molcanther/11/9/1925/F1.large.jpg

Meech
Member
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… Read more »
Meech
Member
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… Read more »
Meech
Member

Update: About 40 mins after taking 150mg dipyridamole, 20mg Simvastatin, 1500mg HCA, I’m fairly lightheaded. I’m assuming this is the dipyridamole.

Tanya
Guest

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…

Alex
Member

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,
Alex

Alex
Member

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

Wondering
Guest

Hi Alex,
sorry to hear that. where did you order Itraconazole from?

Alex
Member

just got it from a local farmacy

Wondering
Guest

No prescription, i know 🙂

Alex
Member

yep, EASY!!!! Like buying bread.

Wondering
Guest

Sigh..i cant buy it here

Alex
Member

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

marcosbomber901
Member
hi Meech. You are so kind as to tell me the dose of Mesna that you administered together to carboplatin.Many thanks for your kindness
Meech
Member

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

marcosbomber901
Member

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

Meech
Member

Maybe daniel can facilitate this because I’d rather not post my email address publicly.

marcosbomber901
Member
Ergin
Member

Hi Marcos,
Did you call the clinic for 3BP+SAL?

marcosbomber901
Member

Hi Ergin

I have not called I’ve been very busy at work ,morning i think i can call.Thank Ergin

Katy
Member
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?… Read more »