The Metabolic Theory of Cancer Explained Podcast Jeffrey Dach MD with Michael Karlfeldt, ND, PhD. Discussing my book, Cracking Cancer Toolkit. Dr. Karlfeldt is an integrative oncologist at The Karlfeldt Center in Meridian, Idaho.

Dr. Karlfeldt: Your book is Cracking Cancer Toolkit. How did you get into writing a book on cancer? And tell us about your background.

Me: Well, I am not an integrative oncologist and I do not see cancer patients in my little office here in Davie, Florida. Rather, I specialize in natural thyroid and bioidentical hormone replacement. I consider myself a “reluctant thyroidologist” because I started doing hormone replacement 20 years ago for menopausal women, and realized, you know what? If I leave the thyroid up to the primary care doctor, they will never do it right. And if I want to get it done right, I have to do it myself.

Link to Podcast behind paywall (only $1.99): I apologize for the paywall which goes to other people to pay for the Cancer Summit. On the good side, it is only 2 dollars! For those who prefer to read, here this is the transcript:

So, back in 1976 to 1980, I did a regular internship, rotated through medicine and surgery at Rush Medical Center in Chicago, and then I did a Radiology residency. And in 1980-1981 then I did an Interventional Radiology fellowship at the University of Miami Jackson Hospital. And then I became board-certified in diagnostic and interventional radiology. And, I worked in the hospital for 25 years in Hollywood, Florida, in the Memorial Hospital System doing both diagnostic and interventional radiology.

And, because I had some eye trouble, I retired about 25 years ago. And then I got a promotion! I started my own little office where we practice outpatient medicine. You know, I sort of returned back to my old days doing internal medicine. So, we mostly specialize in menopausal hormone replacement and natural thyroid. But, as you know, we are a full service medical practice. Our patients may have other medical problems, and we address those as well. Getting back to my book, Cracking Cancer Toolkit. How did I write a book on cancer? Well, during the early days of my little outpatient clinic. three of my close family members contracted aggressive forms of cancer. And so, I realized I had to get up to speed on the new research, because current cancer treatment is, as you know, like we are back in the 1950’s and 1960’s. As you know, chemotherapy really hasn’t changed all that much in 70-80 years. And there has been tremendous advances in cancer research, mostly preclinical in-vitro and also animal xenograft type studies. There is a tremendous amount of money that has gone into research run through the NIH since Nixon started the war against cancer. The NIH has dumped billions into it, and a lot of it is preclinical animal studies. So we have this gigantic volume of research which is largely untapped, and so I learned as much of this material as I could and used it for my three family members with aggressive cancers, and all three had good outcomes. So I thought, you know what? I should write a book about it so everyone else can receive the benefits of this type of book.

One of the things that I learned early on was that chemotherapy treatments will shrink the tumor temporarily, but the net result is that the tumor recurs with a much more aggressive cell type. And the reason for that is that chemotherapy causes a tremendous increase in inflammation, which can be measured with the Cytokine IL-6. This is the one most commonly measured. The inflammatory master controller is the nuclear factor kappa B pathway which is massively upregulated by chemotherapy. The net result of chemotherapy is that in most cases, it makes the cancer worse. After a brief remission, the cancer becomes drug-resistant and much more aggressive, and spreads and becomes metastatic.

Su, Jin-xuan, et al. “Chemotherapy-induced metastasis: molecular mechanisms and clinical therapies.” Acta Pharmacologica Sinica 44.9 (2023): 1725-1736.

Vyas, Dinesh, Gieric Laput, and Arpitak K. Vyas. “Chemotherapy-enhanced inflammation may lead to the failure of therapy and metastasis.” OncoTargets and therapy (2014): 1015-1023.

Karagiannis, George S., John S. Condeelis, and Maja H. Oktay. “Chemotherapy-induced metastasis: molecular mechanisms, clinical manifestations, therapeutic interventions.” Cancer research 79.18 (2019): 4567-4576.

I consider chemotherapy an obsolete technology. The exception is testicular cancer, where the cancer stem cells are sensitive to chemotherapy. And that brings us to the cancer stem cell. What is the reason why cancers recur after chemotherapy? The bottom line is that chemotherapy eradicates the tumor bulk cells, but leaves the cancer stem cells unharmed. The reason for that: the cancer stem cells are hibernating. They are actually dormant, sort of like a hibernating bear in the winter. And they are not actively dividing. So, chemotherapy will target the actively replicating, actively dividing cells in the cancer and also in the human body. And that is the genesis of most of the adverse side effects of chemotherapy. We have rapidly dividing cells in the Gastrointestinal tract, the epithelium will be denuded. Our bone marrow cells are rapidly dividing and so they are also targeted by chemotherapy. Patients receiving chemotherapy will develop anemia and low white count. So the combination of denudation of the epithelial layer of the Gastrointestinal tract from chemotherapy, which causes leaky gut and gram negative endotoxemia (sepsis), you know, that combination, along with leukopenia, a very low white count, that’s a highly fatal combination. You know, septic shock with no white count.

Dr. Karlfeldt: what makes the cancer stem cells get active once the chemotherapy is done?

There are various triggers for cancer cells, for example, lymphoma cells. Lymphomas are known to be dormant. Many of them tend to be slow-growing, which is measured by the KI-67 proliferation marker. Many lymphomas and even breast cancers have a low KI-67.

Dr. Karlfeldt: What triggers them to become more aggressive?

Me: That is a good question. Environmental triggers? One of the triggers is inflammation. Increased inflammation in the body. The vast majority of cancers will become much more aggressive in an inflammatory micro-environment. One of the drawbacks of chemotherapy is that it creates a massively inflammatory microenvironment. The lymphomas, you know, some of them will respond well to chemotherapy and you can have a “cure”, but the aggressive lymphomas will regress and the patient will have a negative PET scan. But then a few months later, the lymphoma comes back with a vengeance, and I believe that’s the inflammatory conditions in the micro-environment created by chemotherapy causing it to come back.

Dr Karlfelt: That makes sense because we know when we have an injury body, lets say hurt knee or something, that triggers an inflammatory response to then signal to stem cells and to other growth factors to get to that location to repair the area. It makes sense that the inflammatory environment in the tumor micro environment, you know, really activates the cancer stem cells to try to heal that damage.

Me: Exactly. That is a good point. So, you know, the other thing perpetuating the chemotherapy paradigm, and it’s amazing how very few people know this, is called the chemotherapy concession. In most of medicine, it is illegal for a doctor to self-refer. For example, when I worked in radiology, I was in a large group, and in our meetings we would talk about how there are laws that prevent us from referring patients to an imaging center that we own. If we own an outpatient imaging center, we can not refer patients to our own center. It is illegal. It’s called the Stark Law. There a number of laws, state and federal, that make it a criminal offense for a doctor to self-refer. These are called anti-kickback laws.
It is illegal for a doctor to receive a kickback. For example, if a refer a patient to a clinic down the street, and ask them for a kickback, you know that patient generates a certain amount of money for that clinic that I refer to, and I ask for a 10 per cent commission, which is commonly done in real estate and other business transactions, but in medicine, that is illegal. And the doctor can go to jail for doing that, receiving a kickback.

A Call to Eliminate ‘Chemotherapy Concession‘ Nick Mulcahy January 02, 2013

Chemotherapy: A financial gain for oncologists Concession Stand by Jenny Thompson
Health Sciences Institute

For some inexplicable reason, the oncologists receive a kickback from the sale of chemotherapy and other oncology drugs. It is called the chemotherapy concession. It has been going on now, going back to the 1960s, 60-70 years. And it is not well known because the mainstream media does not publicize that the oncologists are receiving a kickback. And that is one of the main mechanisms perpetuating an obsolete technology called chemotherapy. It is basically an obsolete technology from the 1950’s.

So I think it should be illegal for oncologists to receive kickbacks. And if you think back, it was common practice for oncologists back 20-30 years ago to do high intensity chemotherapy that would wipe out the bone marrow in women with breast cancer. Because they were receiving a kickback, they wanted to use more and more chemotherapy. The more chemotherapy they used, the more money they would make. So they came up with the idea, well, if we can’t give too much chemotherapy because it wipes out the patient’s bone marrow, and then they die, so let’s do this thing called bone marrow transplantation. We will harvest the bone marrow first, before the patient receives treatment, and then after the bone marrow is totally wiped out and the patient is helpless, they are going to die, they then receive a transfusion of the bone marrow. The patient’s own bone marrow, back into their body , which saves them. And that is the bone marrow transplant for breast cancer. That was done for many years until finally it was studied, it was the subject of 6 randomized controlled trials reported by Dr. Donald Berry in 2011, and they discovered, guess what? Surprise! It has no clinical benefit. And so the whole practice was discredited and they stopped doing it.

Berry, Donald A., et al. “High-dose chemotherapy with autologous hematopoietic stem-cell transplantation in metastatic breast cancer: overview of six randomized trials.” Journal of Clinical Oncology 29.24 (2011): 3224-3231.

Stadtmauer, Edward A., et al. “Conventional-dose chemotherapy compared with high-dose chemotherapy plus autologous hematopoietic stem-cell transplantation for metastatic breast cancer.” New England Journal of Medicine 342.15 (2000): 1069-1076.

You know, you have other problems with conventional oncology. The drug companies decided to invent a recombinant erythropoetin called Procrit and it was approved for kidney failure patients because they would frequently have anemia, and later, was Procrit was approved for the anemia of cancer patients receiving chemotherapy. And the Procrit was given commonly to increase the blood count in chemotherapy patients who had anemia. And they did that for many years until they discovered that the erythropoietin stimulates red cell production, and guess what? Surprise! It also stimulates cancer growth and cancer production, so that was discredited and oncologists stopped using it. They don’t talk about it. It is one of those things that became politically incorrect.

Henke, Michael, et al. “Erythropoietin to treat head and neck cancer patients with anaemia undergoing radiotherapy: randomised, double-blind, placebo-controlled trial.” The Lancet 362.9392 (2003): 1255-1260.

Leyland-Jones, Brian, et al. “Maintaining normal hemoglobin levels with epoetin alfa in mainly nonanemic patients with metastatic breast cancer receiving first-line chemotherapy: a survival study.” Journal of Clinical Oncology 23.25 (2005): 5960-5972.

There is a new drug, granulocyte colony stimulator, GCSF, which stimulates white cell production. And that is still very commonly used in chemotherapy patients because the chemotherapy will wipe out the white cells, and they have leukopenia which is dangerous because they can die of sepsis when the white count is low like that. So they will give them a Neupogen shot, this is the brand name for one of the GCSF drugs which stimulates white cell production.

So the big question is: What is happening to the cancer? If the patient has a leukemia, for example guess what? Leukemias are white cells. And so there a number of studies showing, and you know what, the cancer is probably being stimulated by the Neupogen shot, and they are just willing to accept that in order to avoid the septicemia and septic shock. I think we are going to find over the next few years that this is going to be a real problem because If you ask what will stimulate cancer stem cells and trigger them to grow again? A drug like that, a drug like Neupogen, can do it. That is one of the many problems with conventional oncology. It is really money-oriented, based on a business model. The whole oncology system has got to be 40-60 years behind current cancer research.

Karagiannidis, Ioannis, et al. “G-CSF in tumors: Aggressiveness, tumor microenvironment and immune cell regulation.” Cytokine 142 (2021): 155479.

Morris, K. T., et al. “G-CSF and G-CSFR are highly expressed in human gastric and colon cancers and promote carcinoma cell proliferation and migration.” British journal of cancer 110.5 (2014): 1211-1220.

So you would think that writing a book like this would be difficult. And it was difficult in the sense of learning a new jargon used in the molecular biology of cancer. This is like learning a new language. That was the difficult part. The fun and enjoyable part is we have all of these new cancer treatments that actually do work, and so in the dedication of the book, I made the statement, this book is dedicated to the half a million patients who died last year of cancer and to the half a million patients next year who won’t. And that is where we are at. Using repurposed drugs and understanding the various cancer metabolic pathways, it is now possible to cure cancer.

Michael Kärlfelft: What causes cancer? You have metabolic, trophoblastic, parasitic, genetic, what is your opinion?

Me: When it comes to choosing a combination of drugs, right at the top of the list we have the metabolic disturbance in cancer which was described by Otto Warburg in the early 1920’s. He received the Nobel prize for discovering that cancer cells have a different metabolic set up that is called aerobic glycolysis. We have much better molecular biology tools now. We know that the metabolic derangement involves a translocation of Hexokinase from the cytoplasm of the cell to the mitochondria. These little pores on the surface of the mitochondria are called voltage-dependent anion channels you know, VDAC for short. It is easier to pronounce “VDAC”.

The hexokinase enzyme is the first enzyme step in the metabolism of glucose. The hexokinase II is not the normal hexokinase. It is an embryonic form. So the normal hexokinase is replaced with an embryonic form of hexokinase called hexokinase II (HK-II), and that is translocated to the VDAC. It is not supposed to be there.

Chiara, Federica, et al. “Hexokinase II detachment from mitochondria triggers apoptosis through the permeability transition pore independent of voltage-dependent anion channels.” PloS one 3.3 (2008): e1852.

Krasnov, George S., et al. “Targeting VDAC-bound hexokinase II: a promising approach for concomitant anti-cancer therapy.” Expert opinion on therapeutic targets 17.10 (2013): 1221-1233.

It then influences the mitochondria, and one of the things that it does, it immortalizes the cell. Normally, cells that are damaged or metabolically deranged in any way will undergo programmed cell death, which is called apoptosis. Sydney Brenner and two other doctors who discovered apoptosis received the Nobel prize in medicine. Is it that important. So when the Hexokinase II is relocated to the VDAC, that turns off the ability of the cell to undergo apoptosis, which is controlled by the mitochondria. So now the cancer cell is immortal and can not commit apoptosis.

And simply by a maneuver, a drug or some agent that will detach the Hexokinase II from the VDAC, this will restore the ability of the cancer cell to undergo programmed cell death. So, that is a valid anticancer strategy. There are a number of repurposed drugs that can do that, which we highlight in the book, because you know, they are widely available at the corner drug store. Drugs like fenofibrate and itraconazole. Fenofibrate is an old lipid drug, and itraconazole is an old antifungal drug. Both have been in use for decades. Both of those two drugs, and there are others, we highlight those two because they are widely available, and they will separate the hexokinase II from the VDAC.

When we look at the metabolic pathways, we are interested in eradicating the cancer stem cells. The thing about cancer stem cells is that they have metabolic plasticity which means they can shift their major energy pathway. From the three major energy pathways, they will shift back and forth depending on what is available, depending on what nutients are available, depending what kind of drug treatment.

So some stem cells will use the glycolytic pathway preferentially, which is the Warbug effect originally described by Otto Warburg, and that is this massive utilization of glucose, relatively bypassing the mitochondria. The second major pathway is oxidative phosphorylation through the mitochondria, which is much more efficient. So if a cancer stem cell is mostly using oxidative phosphorylation, and is given a drug that blocks oxidative phosphorylation, that cancer stem cell will then switch to the glycolytic pathway in the cytoplasm.

The third major pathway, which is highly active in cancer stem cells, is called autophagy. Autophagy is ignored by conventional oncology. I discovered the importance of autophagy when I was researching an anti-malaria drug called artemisinin which was actually discovered by the Chinese. There was a Chinese doctor by the name of Too You You, and in 2015, she received the Nobel prize in Medicine for discovering artemisinin, an anti-malaria drug, which is now a first-line treatment. It is given intravenously in third-world countries as first-line treatment for malaria. It turns out that artemisinin is also an excellent anti-cancer drug, as many of the anti-parasitic drugs will have a dual purpose and can be used as anti-cancer drugs very effectively.

Liu, Wenxiu, and Yue Liu. “Youyou Tu: significance of winning the 2015 Nobel Prize in Physiology or Medicine.” Cardiovascular diagnosis and therapy 6.1 (2016): 1.

Tambo, Ernest, et al. “Nobel prize for the artemisinin and ivermectin discoveries: a great boost towards elimination of the global infectious diseases of poverty.” Infectious diseases of poverty 4.1 (2015): 58.

So, when I was reading about the artemisinin, I saw many of these studies are done in-vitro. They also have animal models in which cancer cells are injected into mice. Specifically, with the in-vitro cancer cell cultures, when they add the artemisinin, they can observe the cells under the microscope and they will see the lysosomes migrate from the periphery of the cancer cell towards the center, near the nucleus. That is called protective autophagy. Autophagy is really a process involving the lysosomes, the entire lysosomal system.

Yang, Nai-Di, et al. “Artesunate induces cell death in human cancer cells via enhancing lysosomal function and lysosomal degradation of ferritin.” Journal of Biological Chemistry 289.48 (2014): 33425-33441.

Jerabkova-Roda, Katerina, et al. “Peripheral positioning of lysosomes supports melanoma aggressiveness.” Nature Communications 16.1 (2025): 3375.

Cabukusta, Birol, and Jacques Neefjes. “Mechanisms of lysosomal positioning and movement.” Traffic 19.10 (2018): 761-769.

Lysosomes are the little bags of digestive enzymes and acid. These are acidified little bags that digest old, unwanted proteins and unwanted organelles. Lysosomes are also involved in other processes, for example, Macropinocytosis, which is shared by single-celled organisms like the amoeba. Everybody remembers biology class when they showed you a movie of an amoeba under the microscope, and it looks like “the blob” and it slides around and engulfs its food. You know, it sends out these pods which engulf the food, and then it brings it into the cell and digests it. That is using autophagy of the lysosome system. So, our cells do the same thing.

Tejeda-Muñoz, Nydia, et al. “Wnt canonical pathway activates macropinocytosis and lysosomal degradation of extracellular proteins.” Proceedings of the National Academy of Sciences 116.21 (2019): 10402-10411.

When the cancer cell is dormant, the lysosomes in this entire autophagy system migrate centrally in the perinuclear area where they hibernate. When the cancer cell becomes aggressive, meaning metastatic potential, the lysosomes will then migrate towards the cell membrane, where they can release acid and digestive enzymes into the microenvironment and actually digest the proteins and tissues surrounding the cancer and obtain nutrition that way, just like other organisms and parasites would do. So autophagy pathways are used by the cancer cells, and to eradicate cancer stem cells, we use an autophagy inhibitor.

It turns out that we have a lot of autophagy inhibitor drugs at the corner drug store. For example, some of the antihistamines such as loratidine which accumulates in the lysosomes and inhibits lysosomal function. We also have proton pump inhibitors, antacids like omeprazole which turn off the acid production in the lysosomes. The lysosomes have an ATP-ase pump, this is a molecular machine that makes the acid. The proton pump inhibitor drugs inhibit these ATP-ase pumps. The lysosomes can not make acid and they become dysfunctional.

Some cancers such as leukemias, have unusually large lysosomes, and they are much more sensitive to autophagy inhibitors that cause the lysosomes to become dysfunctional. And that is one of the main mechanisms for artemisinin which accumulates in the lysosomes of the cancer cell which have a very high iron content, a major difference compared to normal cells.

Cancer cells tend to accumulate iron in the lysosomes. The artemisinin has this “peroxide bridge” which is an oxygen molecule “sticking off” the larger artemesinin molecule, ready to react with pretty much anything. So the oxygen will react with the iron in the lysosomes and create ROS, reactive oxygen species, which then cause the lysosomes to burst, releasing its contents, all that acid and “goop” into the cytoplasm, which kills the cancer cell.

Dr. Karlfeldt: What about safety?

Me: Artemisinin (Artusenate) is extremely safe with low incidence of serious adverse effects. Everything is a matter of dosage and iron content. Normal cells do not have the same iron content as cancer cells. That is the main differential feature that protects normal cells. You can reach a toxic dose if you give enough artusenate, obviously. For treatment of malaria patients with IV artusenate, standard dosage is 2.4 mg/kg per dose, administered intravenously at 0 hours, 12 hours, and 24 hours, then once daily thereafter. This is considered very safe.

Some of the other autophagy inhibitors do have more pronounced, more worrisome adverse side effects. For example. there is a whole class of autophagy inhibitor anti-malarial drugs, mefloquine, chloroquine and hydroxychloroquine, all related, and originally from quinine from the cinchona tree. The safest of the three is hydroxychloroquine. The most effective and yet the one with the most adverse side effects is mefloquine which accumulates in the lysosomes and disrupts lysosomal function. It is highly effective and an excellent cancer stem cell agent, an anticancer drug, and also very good anti-malaria drug. The problem is it causes neuropsychiatric disturbances, and brain degeneration in animal studies.

With many of these anticancer drugs, you have to be careful of adverse side effects, especially with the OXPhos inhibitors, oxidative phosphoylation inhibitors tend to be mitochondrial toxins. maybe one agent is fairly safe, like metformin targets Complex One of the Electron Transport Chain.

There are millions of people taking metformin. They do okay with it. But if you add another mitochondrial agent, you know another, or a third, or a fourth, then you start to get more adverse side effects from mitochondrial toxicity.

For example, if you add a statin drug, which is also a mitochondrial toxin. If a statin is added to metformin or another oxphos inhibitor, for example, niclosamide is a mitochondrial uncoupling agent, another antiparasitic drug, commonly used for tapeworm. Niclosamide is a very good anticancer agent because it is both an OXPHOS inhibitor and Autophagy inhibitor. You can add a Glycolysis inhibitor to Niclosamide and you are now blocking all three major pathways, OXPHOS, Glycolysis and Autophagy.

So the idea is to get synthetic lethality, which means you are preventing metabolic plasticity, you are preventing the cancer cell from shifting to a different metabolic pathway, and preventing the cancer cell from defeating the drug cocktail. So, you have to block all three metabolic pathways, OXPHOS, Glycolysis (Warburg Effect) and Autophagy.

The last third of the book is devoted to Inflammation and Immune Evasion.

The cancer cells will hijack the immune system. They make themselves invisible to the immune system. And a lot of treatments are involved in restoring immune surveillance.

The inflammatory pathways are hijacked by cancer cells, and they use that to make themselves more aggressive. We have anti-inflammatory drugs such as celecoxib (Celebrex) and other NSAIDS. Those studies have been done and published showing that if you give Celebrex along with chemotherapy, it downregulates the inflammatory cytokines produced by the chemotherapy, and the patients have better outcomes.

Ye, Shi-Yu, et al. “The efficacy and safety of celecoxib in addition to standard cancer therapy: a systematic review and meta-analysis of randomized controlled trials.” Current Oncology 29.9 (2022): 6137-6153.

The Mouse That Defeated Cancer

Getting back to the immune system, I was intrigued by a research project at Wake Forest Medical School in Winston Salem. They had medical students injecting mice
with cancer cells. This went on for months and months. All the mice died! And then, out of the blue one day, the medical student held up the mouse. This one mouse did not die and was still alive after a cancer injection. They named the mouse the SR/CR mouse, spontaneous regression, complete remission mouse. And they were very excited about finding this mouse that could defeat cancer. And so they did further studies. They asked the question: What if we transfer the SR/CR mouse’s immune system, the T cells, to a normal wild-type mouse? Would that confer protection? Sure enough, they were protected, and that was the beginning of immunotherapy. They were able to transfer the immune system of a cancer resistant (SR/CR) mouse and confer this resistance to a second mouse.

Hicks, Amy M., et al. “Transferable anticancer innate immunity in spontaneous regression/complete resistance mice.” Proceedings of the National Academy of Sciences 103.20 (2006): 7753-7758.

Koch, Janne, et al. “Immune cells from SR/CR mice induce the regression of established tumors in BALB/c and C57BL/6 mice.” PloS one 8.3 (2013): e59995.

Coley’s Toxins

The doctor who really pioneered immunotherapy in the early 1900’s was an orthopedic surgeon in New York City by the name of William Coley. In those days, they didn’t have much to offer. The big cancer of the bone was osteosarcoma, and it still is. Dr. Coley did 100 amputations for osteosarcoma. One of the patients was a young female patient with an osteosarcoma of the hand. Dr Coley did an amputation of the hand, and the patient died a few months later of metastatic disease. He was so distraught that he reviewed the last 100 cases he operated on. There was only one survivor. And he noticed in the chart that this survivor had a postoperative strep infection. And so he speculated that
the bacterial infection must have stimulated the immune system, and that’s what made the difference in that one surviving patient. So, he came up with a concoction of bacterial toxins. It was dubbed Coley’s Toxins, named after him, and he would inject these toxins into the cancer patients. Not everybody, of course, had remissions, but there were many remarkable remissions that he published in the medical literature of his day. And of course, when chemotherapy was invented, that is when the FDA closed down Coley’s toxins.

Coley was one of the pioneers and now, current day immunotherapy is done with checkpoint inhibitors. The problem with checkpoint inhibitors is they don’t work on everybody. If they do work, patients develop drug resistance fairly quickly. There was a mad rush to find out how to make the checkpoint inhibitors work better. The discovery was made, guess what? it is the microbiome. You know, the friendly bacteria in the gut that make the immunotherapy work. And how did they discover that?

The Year of the Microbiome

It is very, very common for chemotherapy patients to develop sepsis because of the low white count and the leaky gut. And so it is very common for them to receive antibiotics. So they looked back and saw that in the patients who received antibiotics that wiped out the microbiome, they did not do well with the checkpoint inhibitors. So they did further studies and sure enough, there are certain bacterial strains in the microbiome that make the checkpoint immunotherapy work. That was discovered in 2017, the year of the microbiome.

Cimetidine

Another surprising discovery that was made in the 1980’s or early 1990’s regarding immunotherapy was that there were case reports of gastric lymphoma cases. They would do upper endoscopy and see a big ulcerated mass in the stomach. Biopsy shows lymphoma. They couldn’t operate right away because the patient had a huge ulcer, so they would treat the patient with an antacid drug for 6 weeks and then operate. In those days, the anti-ulcer drug was Tagamet, the brand name for cimetidine, which is actually an antihistamine-type drug and an anti-acid. Since then, Cimetidine has been replaced by the newer PPI drugs. Cimetidine is still available over the counter at the corner drug store. They noticed in these two cases where the patients were treated for six weeks with Cimetidine, they go in to do the operation and they find the ulcer is gone, and rebiopsy shows the lymphoma is totally GONE! So they realized that the Cimetidine cured the lymphoma cancer.

Sure enough when you do the pre-clinical studies, Cimetidine upregulates the immune system, a valid anticancer strategy. In addition, Cimetidine upregulation of the immune system can be used for anti-viral treatment.

Cimetidine for Cutaneous Warts

For example, there was a series published on the medical literature on 8 children who received a heart transplant for whatever reason. 7 out of the 8 had complete resolution of recalcitrant cutaneous warts on cimetidine. They give immunosuppressive drugs to prevent rejection. And because they are immunosuppressed, the children are prone to re-activated viral disease that can go rampant. The common is a strain of HPV, human papilloma virus which causes warts on the fingers that grow into long protruding growths, warts, on the tips of the fingers. They showed them with photographs in the journal. You cant miss it . It is very obvious. One of the doctors had the bright idea of giving Cimetidine to the children with the viral warts, and 7 of the 8 children cleared up with cimetidine because of upregulation of the immune system. That gives you an idea of what an over-the-counter repurposed drug can do to boost the immune system. Used along with other repurposed drugs as a complete program, everything is additive, and it does help.

references:

Das, Bibhuti B., et al. “Cimetidine: a safe treatment option for cutaneous warts in pediatric heart transplant recipients.” Medical Sciences 6.2 (2018): 30.

Tan, Sien Hui, et al. “Cimetidine for recurrent respiratory papillomatosis in pregnancy as an alternative adjuvant treatment.” European Archives of Oto-Rhino-Laryngology 281.2 (2024): 1053-1055.

Levy, D. W., A. K. Banerjee, and Helen P. Glenny. “Cimetidine in the treatment of herpes zoster.” Journal of the Royal College of Physicians of London 19.2 (1985): 96.

Beta Glucans / AHCC

The other available immune stimulator, widely available over the counter, is called beta-glucan at the health food store. It is a long chain sugar-like molecule found in cereals, certain mushrooms, yeast and other foods. These have a molecular pattern which mimic pathogenic patterns, pathogenic pattern mimicry. These are called Pathogen-Associated Molecular Patterns (PAMPs) which stimulate the immune system of the patient.

Out of a number of case reports, the one I remember from the book is an elderly man in his late 70’s with metastatc prostate cancer to the bones. The doctors tried everything, every conventional treatment you can imagine, and it is finally refractory to all treatments. His PSA is sky high, like 1100. The patient declines all further treatment and instead takes one of these beta-glucan products. The most popular one is called AHCC, a product from Japan. 6-8 weeks later the PSA has come down dramatically, and he is feeling much better and exercising. That is a dramatic case report of success with upregulating the immune system with a beta glucan type product. That is very impressive.

Wu, Lijuan, et al. “Antitumor effect of soluble β-glucan as an immune stimulant.” International journal of biological macromolecules 179 (2021): 116-124.

Mishra, Vartika, et al. “Beta glucan as an immune stimulant in tumor microenvironment—Insight into lessons and promises from past decade.” International Journal of Biological Macromolecules 234 (2023): 123617.

McFarlin, Brian K., et al. “Discovery of Innate Immune Response mRNAs That Are Impacted by Structure-Specific Oral Baker’s Yeast Beta Glucan Consumption.” BioTech 14.1 (2025): 4.

Stephen Bigelsen, M.D

There a lot of these very impressive case reports in the medical literature. The other one that was very impressive, I thought, was Steven Bigelsen, a doctor at Cornell Medical Center who in 2016, comes down with metastatic pancreatic cancer.  And he was a smart guy. He realized that prognosis with chemotherapy was not good, so he researched the medical literature and devised his own program, which was a high dose vitamin D analog called paricalcitol, hydroxychloroquine, intravenous vitamin C, statins, metformin, curcumin, and aspirin. And he is now cancer-free and is still alive. I looked it up. He is still alive, 10 years later! That is a really remarkable story.

Bigelsen, Stephen. “Evidence-based complementary treatment of pancreatic cancer: A review of adjunct therapies including paricalcitol, hydroxychloroquine, intravenous vitamin C, statins, metformin, curcumin, and aspirin.” Cancer management and research (2018): 2003-2018.

There are a couple of cancer survivors who inspired my book. One is Ben Williams who wrote: Surviving Terminal Cancer published in 2002. He was a psychology professor at U of Cal San Diego, close to the border with Mexico. This was before the internet, so he would do his research in the University medical library and then drive across the border into Mexico to buy the repurposed drugs. One of them was Accutane, a vitamin A derivative used for acne. He came up with an entire cocktail of repurposed drugs and he is still alive today after a diagnosis of glioblastoma, a brain tumor which is invariably fatal. His book was one of the inspirations for my book.

Partial List of Repurposed Drugs Used by Ben Williams (from his book):

Accutane (Isotretinoin) (Vitamin A derivative)
Celebrex (Celecoxib): COX-2 inhibitor, NSAID anti-inflammatory drug.
Fenofibrate: old lipid drug
Chloroquine: An antimalarial drug autophagy inhibitor.
Metformin: Diabetes drug, OxPhos Inhibitor,
Cimetidine: An H2 receptor blocker for ulcers, to upregulate immune response, Melatonin, PSK (a Turkey Tail mushroom extract): β-glucans, standard treatments ( temozolomide, radiation, neurosurgery )

Jane McClellan Starving Cancer

And the other inspiration is Jane McClellan’s book, Starving Cancer. I met Jane McClellan at the Annie Appleseed meeting one year in West Palm Beach, which is not too far from my office in Davie, Florida. So I was able to drive there to the meeting.

Joe Tippens and Fenbendazole

I also met Joe Tippens at the same meeting. They were both there. Joe was a cattle rancher in Oklahoma in 2017 when he came down with small cell lung cancer with extensive metastatic spread. Joe was treated at MD Anderson in Texas with an experimental immunotherapy drug, and sent home with a poor prognosis. Once home, a veterinarian friend told him to try fenbendazole, a veterinary dog dewormer, which he took along with Vitamin E, Curcumin and CBD oil. 3 months later, repeat PET scan at MD Anderson showed he was cancer free, the only one of 1,100 patients in the immunotherapy clinical trial using pembrolizumab (Keytruda) that survived.

Fenbendazole, a veterinary drug, is not approved for human use. The drug is widely available at pet stores, and is similar in molecular structure to mebendazole, which is FDA approved for human use. Both drugs are microtubule inhibitors which is an entire class of anticancer drugs.

Fenbendazole Combined with Ivermectin

Some integrative oncologists are combining Fenbendazole (or mebendazole) with Ivermectin for synergistic effect. Partial list: William Makis MD, Paul Marik MD, Dr. Ilyes Baghli, MD, Jason R. Williams, MD, Pierre Kory, MD, Imran Khan, MD

Those are the inspirations for my book. If these types of approaches are widely adopted, I think we are going to see a huge turnaround in cancer in the country. It is integrative oncologists who are leading the way with that.

Get Your List of Integrative Oncologists

As I said earlier, I don’t treat cancer patients myself in my own practice. I do not treat cancer patients. I don’t see cancer patients regularly. It is not my specialty. And so we have a list of integrative oncologists, which we provide to anyone who calls the office interested in treatment. For any one interested in the list of integrative oncologists, contact me at my contact page for the List. We will be happy to send you our list.

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Published on September 12th, 2025 by Jeffrey Dach MD