Category: News

Understanding Pharmaceutical Standard, Food Grade and Feed Grade

While supplements aren’t necessary to add to the COC Protocol, we know many of our patients are interested in them.

Care Oncology patients will now be able to order supplements that meet pharmaceutical standards.

pharmaceutical reference standard is a highly characterized material suitable to test the identity, strength, quality and purity of substances for pharmaceutical use and medicinal products.

Our oncologists and nurses are happy to help with any potential interactions of supplements and medications.

Pharmaceutical standard supplements are available through Pharmacy Solutions HERE.  Use code COC2021 for patient pricing.

Why Combine the COC Protocol with Standard of Care?

To maximize potential benefits of the COC Protocol, we recommend taking the Protocol in combination with standard cancer treatments where possible.

We designed the COC Protocol for use alongside all standard cancer treatments, including radiotherapy, chemotherapy, hormonal treatments, and newer therapies (e.g., immunotherapies, targeted therapies). Numerous laboratory-based scientific studies support this approach, and reported results suggest that the COC Protocol medications may help to improve the effectiveness of standard treatments in several different ways:

  • Metformin Along with ‘metabolically reprogramming’ cancer cells to make them potentially more vulnerable to standard of care treatments, metformin may also help to sensitize tumor response to standard therapies by: targeting generally harder to treat cancer stem cells, improving the hypoxic (low-oxygen) state which can often develop around tumors and which hinders the effectiveness of standard treatments, reversing multidrug resistance in cancer cells, and by beneficially modulating the tumor microenvironment (Tang et al, 2021, Jin et al, 2020).
  • Statins can improve the radiation sensitivity of cancer cells grown in the lab by increasing production of cell-damaging oxidative stress molecules (Hosseinimehr et al., 2020). Lab studies also show that statins can help reduce chemotherapy resistance in various different cancer cell types by targeting molecular processes in these cells- including blocking HMG-CoA reductase-dependent molecular pathways (Chen et al 2013, Chen et al, 2012).
  • Mebendazole may help to sensitize cancer cells to radiation therapy by increasing radiation-induced DNA damage. The drug can also work alongside chemotherapy drugs, overcoming cancer cell resistance (Guerini et al, 2019).
  • Doxycycline can help sensitize cancer cells to radiation by decreasing levels of a cell molecule called DNA-PK. Cancer cells are known to need this molecule for DNA repair, and it has been linked to radiation resistance in cancer cells (Lamb et al, 2015). Similar to metformin, doxycycline may also target cancer stem cells in low-oxygen areas that are resistant to traditional chemotherapies, and disrupt the molecular mechanisms that cancer cells use to produce energy (Tan et al, 2017 and De Francesco et al, 2017).

Numerous epidemiological studies support these preclinical potentiation/sensitization findings, as do small clinical studies in patients with cancer. In addition, the extensive evidence base which supports the overall use of the COC Protocol in cancer also includes more extensive epidemiological studies, and a growing number of human clinical trials across a wide range of cancer types.

To get the most out of the COC Protocol, we encourage you to always investigate any standard of care therapy options which may be available to you, whatever your situation now, or in future.

The COC Medical Team are with you every step of the way. As your standard of care treatments and other circumstances evolve over time, our doctors expertly tailor refinements to your Protocol to maximize safety, tolerance of treatment and the potential for positive outcomes.

Selection of Studies

Potentiation of Radiotherapy

Med Paper Conclusions (adapted from paper abstract)
Met and Stat Statin and metformin therapy in prostate cancer patients with hyperlipidemia who underwent radiotherapy: a population-based cohort study

Li et al., 2019

(Observational patient study)

Study results link the use of statins or metformin after prostate cancer diagnosis with increased survival in patients with hyperlipidemia and radiotherapy.
Met Radiosensitization of pancreatic cancer cells by metformin through the AMPK pathway.
Fasih et al., 2014

(Lab-based cell study)

Study findings suggest that metformin can help to radiosensitize pancreatic cancer cells through the molecular ‘AMPK pathway’, and may also affect how cancer cells repair their damaged DNA. These data indicate that metformin may increase the effectiveness of radiation therapy for pancreatic cancer.
Met Effect of mitochondrial metabolism-interfering agents on cancer cell mitochondrial function and radio/chemosensitivity
Mitrakas et al., 2014
(Lab-based cell study)

Study concludes that amiodarone and metformin deserve further experimental and clinical evaluation as cancer cell sensitizers to chemotherapy and radiotherapy.
Met Antidiabetic Biguanides Radiosensitize Hypoxic Colorectal Cancer Cells Through a Decrease in Oxygen Consumption
De Mey et al., 2018
(Lab-based cell study)
Study results demonstrate that metformin and phenformin can overcome hypoxic (low-oxygen) induced cancer cell resistance to radiotherapy by decreasing the cell’s need for oxygen to generate energy. These results provide a rationale to explore metformin and phenformin as hypoxic radiosensitizers.
Stat Atorvastatin Sensitizes Breast and Lung Cancer Cells to Ionizing Radiation

Hosseinimehr et al., 2020
(Lab-based cell study )

Atorvastatin increased cell-damaging ROS (reactive oxygen species) production in irradiated cells. The study demonstrates that atorvastatin has a radiosensitizing effect on breast and lung cancer cells through increasing programmed cell death (apoptosis), ROS production and cell death induced by ionizing radiation.
Stat Clinical Potential of Statins in Prostate Cancer Radiation Therapy

Hutchinson and Marignol, 2017

The literature supports the radiosensitizing properties of statins and their potential antitumor effects in prostate cancer. conflicting study results still need to be understood, however
Meb Mebendazole Potentiates Radiation Therapy in Triple-Negative Breast Cancer

Zhang et al., 2018
(Lab-based cell study)


Mebendazole (MBZ) efficiently depletes the no. BCIC (breast cancer initiating cells) and prevents the ionizing radiation–induced conversion of breast cancer cells into therapy-resistant BCICs. MBZ sensitizes triple-negative breast cancer (TNBC) cells to ionizing radiation in the lab and in animal studies, resulting in improved tumor control in a small animal model of TNBC.
Meb Microtubule-targeting agents can sensitize cancer cells to ionizing radiation by an interphase-based mechanism

Markowitz et al, 2017

(Lab-based cell study)

This study demonstrates that MBZ can sensitize cancer cells to ionizing radiation using mechanisms independent of the induction of growth arrest. In addition, evidence is provided supporting the hypothesis that [MBZ]-induced radiosensitization is mediated by blocking accumulation of DDR protein in the cell nucleus.
Meb Mebendazole as a Candidate for Drug Repurposing in Oncology: An Extensive Review of Current Literature
Guerini et al., 2019
Mebendazole not only exhibits direct cytotoxic (cell-killing) activity, but also works alongside ionizing radiations and different chemotherapeutic agents and stimulates antitumoral immune response.
Doxy Doxycycline down-regulates DNA-PK and radiosensitizes tumor initiating cells: Implications for more effective radiation therapy.
Lamb et al., 2015
(Lab-based cell study)
Study shows that doxycycline effectively inhibits the mammosphere-forming (stem-cell) activity of patient breast cancer cell samples taken from metastatic disease sites. Our results also have possible implications for the radio-therapy of brain tumors and/or brain metastases, as doxycycline is known to effectively cross the blood-brain barrier.


Potentiation of Chemotherapy

Med Paper Conclusion
Met The Chemosensitizing Role of Metformin in Anticancer Therapy (Review)

Tang et al., 2020


A growing body of evidence indicates that metformin can sensitize tumor responses to different chemotherapeutic drugs, such as hormone modulating drugs, anti-metabolite drugs, antibiotics, and DNA-damaging drugs via selective targeting of cancer stem cells, improving the hypoxic (low-oxygen) microenvironment, and by suppressing tumor metastasis and inflammation.
Met Real-time assessment of platinum sensitivity of primary culture from a patient with ovarian cancer with extensive metastasis and the platinum sensitivity enhancing effect by metformin

Liu et al, 2018
(Cell Study)

Metformin rapidly increased the sensitivity of cells to platinum‑based chemotherapy, and this effect was dose‑dependent. The effect of metformin on chemotherapeutic sensitization of cancer cells is clear in vitro, and the real‑time cell analyzer assay has the potential to assist in determining individualized drug regimens for patients with metastatic ovarian cancer.
Met Therapeutic metformin/AMPK activation blocked lymphoma cell growth via inhibition of mTOR pathway and induction of autophagy

Shi et al., 2012
(Lab-based cell study)

Combined treatment of oral metformin with doxorubicin or temsirolimus triggered lymphoma cell autophagy and functioned more efficiently than either agent alone. Taken together, these data provided first evidence for the growth-inhibitory and drug-sensitizing effect of metformin on lymphoma.
Met Association of p53 and mitochondrial gene with chemosensitization by metformin in ovarian cancer
Wei et al., 2018
(Lab-based cell study)
Metformin enhances the sensitivity of drug-resistant ovarian cancer cells to chemotherapy.


Stat Anti-tumor effects of statins in triple-negative breast cancer: Apoptosis, chemosensitization and degradation of mutant-p53

O’Grady et al., 2020

DOI: 10.1158/1538-7445.AM2020-1775
(NB non-peer-reviewed abstract)

(Lab-based cell study)

Combination treatment of simvastatin and the chemotherapeutic agents doxorubicin or docetaxel showed synergistic growth inhibition (in triple-negative breast cancer cell lines).
Stat Statin therapy is associated with improved pathologic response to neoadjuvant chemoradiation in rectal cancer

Mace et al., 2013

(Retrospective patient study)

Statin therapy linked to an improved response of rectal cancer to neoadjuvant chemoradiation. These data provide the foundation for a prospective clinical trial.
Doxy Targeting hypoxic cancer stem cells (CSCs) with Doxycycline: Implications for optimizing anti-angiogenic therapy

De Francesco et al., 2017

(Lab-based cell study)

Doxycycline effectively targets the sub-population of hypoxia (low oxygen)-induced cancer stem cells (CSCs) that are paclitaxel-resistant, overcoming hypoxia-induced drug-resistance. Anti-angiogenic therapy often induces tumor hypoxia, allowing CSCs to survive and grow, ultimately driving tumor progression. Therefore, this study suggests that doxycycline could be used in combination with anti-angiogenic agents, to actively prevent or minimize hypoxia-induced treatment failure.
Doxy Induction of Mitochondrial Dysfunction and Oxidative Damage by Antibiotic Drug Doxycycline Enhances the Responsiveness of Glioblastoma to Chemotherapy
Tan et al., 2017

(Lab-based cell study)

Study shows that doxycycline is effective in targeting glioblastoma through inducing mitochondrial (cell-battery) problems and causing oxidative stress.
Meb Anthelmintic mebendazole enhances cisplatin’s effect on suppressing cell proliferation and promotes differentiation of head and neck squamous cell carcinoma (HNSCC)
Zhang et al., 2017

(Lab-based cell study)

Mebendazole works alongside cisplatin in suppressing cell growth and division and inducing apoptosis of human HNSCC (Head and neck squamous cell carcinoma) cells.


Overcoming Chemo/Radio resistance

Med Paper Conclusion
Met & Stat Combination simvastatin and metformin induces G1-phase cell cycle arrest and Ripk1- and Ripk3-dependent necrosis in C4-2B osseous metastatic castration-resistant prostate cancer cells
Babcook et al., 2014
(Lab-based cell study)
The cell death-inducing capacity of simvastatin and metformin may make these drugs a highly effective treatment for apoptosis (programmed cell death) and chemotherapy-resistant metastatic castration-resistant prostate cancer cells.
Met Metformin inhibits the development, and promotes the resensitization, of treatment-resistant breast cancer
Davies et al, 2017
(Lab-based cell study)
Demonstration that metformin can prevent multidrug resistance (MDR) development and resensitize MDR cells to chemotherapy in vitro, provides medical relevance towards metformin’s potential clinical use against MDR cancers.
Met Metformin reverses multidrug resistance and epithelial-mesenchymal transition (EMT) via activating AMP-activated protein kinase (AMPK) in human breast cancer cells
Qu et al, 2014
(Lab-based cell study)
Metformin can resensitize multidrug-resistant breast cancer cells due to activating the molecular AMPK cell pathway.
Met Metformin sensitizes hypoxia-induced gefitinib treatment resistance of HNSCC via cell cycle regulation and EMT reversal
Yin et al., 2018
(Lab-based cell study)
Study shows metformin sensitizes HNSCC (head and neck squamous cell carcinoma) to gefitinib treatment, which might serve as a novel combined treatment strategy.
Met Metformin sensitizes endometrial cancer cells to chemotherapy through IDH1-induced Nrf2 expression via an epigenetic mechanism.
Bai et al, 2018
(Lab-based cell study)
Findings suggest that rational combination therapy with metformin and chemotherapeutics has the potential to suppress chemoresistance.
Stat Atorvastatin overcomes gefitinib resistance in KRAS mutant human non-small cell lung carcinoma cells

Chen et al., 2013
(Lab-based cell study)

Atorvastatin overcomes gefitinib resistance in KRAS mutant non-small cell lung carcinoma cells through inhibition of HMG-CoA reductase-dependent molecular pathways.
Stat Atorvastatin sensitizes human non-small cell lung carcinomas to carboplatin via suppression of AKT activation and upregulation of TIMP-1

Chen et al., 2012
(Lab-based cell study)

Data demonstrate that atorvastatin may overcome carboplatin resistance in lung cancer by suppressing molecular AKT activity and increasing TIMP-1. A combination of atorvastatin and carboplatin may be an effective strategy in clinical therapy against  non-small cell lung carcinomas.
Stat Simvastatin Sensitizes Radioresistant Prostate Cancer Cells by Compromising DNA Double-Strand Break Repair
Chen et al., 2018
(Lab-based cell study)
Results demonstrated that a combination treatment with simvastatin and ionizing radiation synergistically induced programmed cell-death of radioresistant prostate cancer cells.
Meb Mebendazole is a potent inhibitor to chemoresistant T cell acute lymphoblastic leukemia cells

Wang et al., 2020

(Lab-based cell study)

This study demonstrated, for the first time, that mebendazole could inhibit chemoresistant T-cell acute lymphoblastic leukemia cells both in the lab and in mice, and the Notch1 molecular cell pathway was suppressed by mebendazole treatment.
Meb The repurposed anthelmintic mebendazole in combination with trametinib suppresses refractory NRASQ61K melanoma.
Simbulan-Rosenthalet al (2017)
(Lab-based cell study)(Cell Study)

These data suggest that mebendazole could be considered as a therapeutic option in combination with trametinib, for patients with NRASQ61mutant or other non-V600E BRAF mutant melanomas.



Potentiation of immunotherapies, targeted therapies & hormone therapies

Med Paper Conclusion
Met Efficacy of metformin in combination with immune checkpoint inhibitors (anti-PD-1/anti-CTLA-4) in metastatic malignant melanoma

Afzal et al., 2018

(Observational Patient Study)

Study observed favorable treatment-related outcomes (including median progression free survival and median overall survival) in patients who have received metformin in combination with immune checkpoint inhibitors (ICIs) without reaching significance, probably, due to small sample size. Hence, large prospective clinical trials are required to study the effect of metformin in combination with ICIs before it can be recommended as routine additive therapy.
Stat and met The updated landscape of tumor microenvironment and drug repurposing

Jin et al, 2020

Discusses how statins and metformin may help to beneficially modulate the tumor microenvironment (which could be potentially beneficial alongside immunotherapies)
Doxy Potential for enhanced therapeutic activity of biological cancer therapies with doxycycline combination
Tang et al, 2013
(Lab-based cell study)
Doxycycline enhanced the replication of an experimental viral-based cancer vaccine in many tumor cell lines, leading to increased sensitivity to these therapies. These therapies used in conjunction with doxycycline led to increased anti-tumor effects. The unexpected and pleiotropic beneficial anti-tumor effects of doxycycline on both immune cell and cancer vaccine therapies make it an excellent candidate for rapid clinical testing.
Met Phase II study of medroxyprogesterone (MPA) plus metformin as a fertility-sparing treatment for atypical endometrial hyperplasia and endometrial cancer.
Mitsuhashi et al, 2016
(Small patient trial)
Metformin inhibited disease relapse after MPA therapy. The combination of metformin and MPA in endometrial cancer treatment should be studied further.
Stat Statin use and survival in patients with metastatic castration-resistant prostate cancer (mCRPC) treated with abiraterone or enzalutamide after docetaxel failure: the international retrospective observational STABEN study
Gordon et al (2018)
(Retrospective patient study)
In this retrospective cohort of 598 patients treated with second-line abiraterone or enzalutamide after docetaxel for metastatic castration-resistant prostate cancer, statin use was significantly associated with both prolonged overall survival and cancer-specific survival and increased early > 30% PSA declines. A clinical trial is now needed.
Met Isolated and combined action of tamoxifen and metformin in wild-type, tamoxifen-resistant, and estrogen-deprived MCF-7 cells
Berstein et al., 2011
(Lab-based cell study)
Metformin interacts additively with tamoxifen to reduce tumor cell growth.


The Metabolism-Cancer Connection & How to Treat It – Dr. Charles Meakin with Dave Asprey – #801

Repurposing existing drugs shows promise in treating the metabolic disruption common to virtually all cancers.

In this episode of Bulletproof Radio, my guest approaches cancer much differently than mainstream medical thinking.

Dr. Charles Meakin is Chief Medical Officer for Care Oncology Clinic USA and works specifically on metabolic treatment strategies for curing cancer. He’s also a career biohacker-physician focused on alternative and holistic treatment strategies that he hopes will shape the “fourth field of cancer care.”

Listen Now…

Mebendazole or Fenbendazole

Many prospective and existing patients ask us about Fenbendazole, which is in the same family of drugs (the Benzimidazoles) as Mebendazole. While there is some interesting preliminary anticancer data associated with Fenbendazole, the drug is not licensed for use in humans. Therefore, long term safety consequences are not yet known, and we have already seen numerous reports of significant liver function abnormalities in patients taking Fenbendazole. There is also a barrier to further developing the evidence base in cancer as human clinical studies cannot be undertaken.

At COC, our team has carefully reviewed all the Benzimidazoles. We have selected Mebendazole in the COC protocol because it: 1. has a human license 2. is already demonstrated as safe in humans 3. is already demonstrated as safe in humans with cancer 4. has the right anticancer mechanisms of action 5. has a significant amount of clinical data in cancer 6. has cancer data that is covered by the existing dosage schedule 7. can be prescribed and monitored by clinicians 8. has the largest amount of scientific and medical data on its use in cancer.

The other Benzimidazole drugs may have utility in cancer, but it is only Mebendazole that satisfies all our criteria for safety and efficacy data and history of use.

We also use Mebendazole Polymorph C, which has been shown to have the best absorption.

The COC Protocol:

Diagram of cell breaking down each part's capabilities

Research on use of statins in cancer

Our nurses have recently received several questions related to statins, one of the medications in the COC Protocol. The following section of our January 2021 newsletter discusses the research literature relating to statins in the context of cancer and addresses some issues raised by a particular journal paper some patients have enquired about.

Statin safety profile

Statins have a good and well understood safety profile in humans. Like all medicines, they may give rise to side effects in some patients, but most people tolerate them well and do not have any problems. Patients often express concerns about the possibility of statin-induced muscle pain, but the actual risk is about 5% or less compared with placebo (a pill that does not contain any medication). Incidence of liver adverse reactions is also quite rare, at less than 2%.

The fact some level of risk exists is precisely why Care Oncology checks bloodwork at baseline and at regular intervals, and monitors for possible side effects. Our team will adjust the dose of statin or pause it if we become aware of any concerns. And of course, we take the same approach with all the other COC protocol drugs too.

Care Oncology’s clinical experience with our patients to date is in line with the risk profile outlined above i.e. the vast majority can tolerate statins without any issues. Blood cell counts and organ function abnormalities are most frequently linked to chemotherapy and/or other conventional care treatments which carry a greater toxicity risk than any of the COC Protocol medications.

Research on use of statins in cancer

Very large numbers of cancer patients take both a statin and metformin for management of other long-term health conditions and need to remain on these drugs for the duration of their cancer treatment. Therefore, a great deal of accumulated safety data exists on their use alongside standard of care cancer therapies, spanning chemotherapy, hormone therapy, targeted therapy, and immunotherapy.

Numerous studies have also shown statins can help to improve the effectiveness of conventional cancer therapies such as chemotherapy and radiotherapy and may help reduce the development of resistance to standard treatments.

In addition, there is now emerging data on the potential for statins to exert protective effects on the heart in patients undergoing chemotherapy.

Due to the high numbers of cancer patients taking a statin for other health conditions, it has been possible to conduct large retrospective studies to explore their impact on cancer incidence and outcomes across different cancer types. These studies have been encouraging and therefore acted as a catalyst for further research, including a growing number of human trials.

Lipophilic statins

The overall data is particularly compelling on the beneficial effects of fat-soluble lipophilic statins in cancer, rather than water-soluble hydrophilic statins.  In addition, lipophilic statins cross the blood-brain barrier more readily.  Atorvastatin, simvastatin and pitavastatin are lipophilic statins, whereas rosuvastatin, pravastatin and fluvastatin are more hydrophilic. As a lipophilic statin, atorvastatin has been extensively explored in the context of cancer and has been generally shown to have superior anticancer effects at the cellular level compared to other less fat-soluble statins. It also has the most extensive safety database due its widespread use for its labelled indication, and allows for dose escalation (as tolerated) to the highest dose achievable.

The power of statins in combination with other medicines

Recent research has demonstrated the potential for enhanced benefit from statins alongside other off-label medicines. e.g. statin + metformin in prostate cancer and endometrial cancer, and statin + metformin + NSAID in lung cancer.

Such studies support the scientific approach at the core of Care Oncology, namely that multiple points of intervention are likely to be needed for a metabolically targeted therapy to have the potential to be truly effective. This is the reason we devised a coherent combination of medicines to address related mechanisms involved in cancer cell metabolism. In this way, the activity of each drug, when given in combination, can potentially produce a synergistic effect and agents do not interfere with or impede one another.

COC Protocol Medications – Mechanisms of action

Diagram of cell breaking down each part's capabilities

A word on contradictory/inconclusive studies

We chose the combination for the COC Protocol carefully – because of the wealth of data in cancer and the safety profile of the medicines separately, together and with standard of care therapies.

This level of safety and efficacy data does not exist for most other off-label medicines, particularly in a combination setting.

We believe it is important to assist our patients to assess different types of evidence and the likely significance of reported results. Fundamentally, our position is that limited pre-clinical data in isolation should be approached with caution – the pharma industry writes off billions of dollars annually in the quest to translate lab studies in rodents to relevant findings for safe and effective treatment of humans.

Recently, several patients have asked us to comment on this paper: Statins have biphasic effects on angiogenesis (Weis et al 2002)

In response to this, we would make the following points:

  • Since 2002 there has been a wealth of supportive published papers on the potential of statins in numerous cancers, especially as regards lipophilic statins (e.g. Atorvastatin) and including human clinical trials.
  • The study referenced is 18 years’ old and laboratory based, in mice. To use mouse body weight as a direct extrapolation to humans is simplistic and inaccurate and human dosing is never based on preclinical research. Without corroborating human data, it is not possible to draw firm conclusions on the possible effects of statins on angiogenesis or any other potential mechanisms relevant in an anticancer setting.

Doses of all medications in humans must be titrated to the individual to avoid toxicities. In the case of Atorvastatin, 40mg once a day is considered a potent therapeutic dose.

  • A common feature of contradictory or inconclusive studies is that frequently they do not research the drug in question alongside standard of care therapies and/or they consider it as a single agent rather than deployed as one component of a coherent metabolically targeted combination.
  • Some cancer research on single agent statin does suggest a greater potential for overall anticancer therapeutic benefit at higher doses, which is why we seek to establish patients at 40mg Atorvastatin daily wherever safe to do so, rather than prescribing a lower dose. Use of Atorvastatin also allows for the possibility of escalating further to 80g daily depending on tolerance, satisfactory lab values and consideration of standard of care therapies and other concomitant medication.

Where it is not a suitable for a patient to be on a 40mg daily dose, our clinicians may still consider a lower dose to be worthwhile, again keeping in mind the principle that the potential for therapeutic benefit is amplified by the combination of medicines.

  • It is key to remember that all the COC Protocol medicines have multi-faceted effects in cancer and that we are using them in combination with standard of care therapy and with each other. Both Mebendazole and Metformin also demonstrate the potential to inhibit angiogenesis.

Further information

Visit our website to read more about statins and the other COC Protocol medications in the context of specific cancer types – – Click on “COC – Select Cancer Types” from the homepage menu

Click here to read our research paper published in Frontiers which provides more detail on our approach and includes preliminary results for our Glioblastoma IV brain tumor cohort.

How could the COC Protocol help you? – Metastatic Breast Cancer

This month’s newsletter features a documentary charting the journey of one of our patients with metastatic breast cancer.

Early in 2018, Yvonne was diagnosed with stage IV breast cancer with multiple metastases in her liver. Faced with a bleak prognosis, she began to research what else she might be able to do in addition to her standard treatment to increase the odds of a positive outcome.

She found Care Oncology and was able enroll on our adjunctive metabolic treatment program designed to complement her conventional care. She also made changes to diet and nutrition and other aspects of her lifestyle.

Yvonne’s daughter Georgia works as a TV researcher and broadcast journalist in London, UK and in 2019 they made a documentary film about Yvonne’s journey. Here’s what Georgia has to say about her mother and the film they made together:

“By using cheap, existing drugs in combination with the conventional cancer treatments, alongside changes to diet and nutrition, we believe mum is living a healthier life with cancer than she was before her diagnosis. This documentary investigates all aspects of “starving cancer” and speaks to those who swear by it, as well as those who totally refute it.”

November 2020 – Zoom update with Yvonne & Georgia

Yvonne and Georgia caught up with Yvonne’s Care Oncology physician, Dr Ndaba Mazibuko, just before Thanksgiving. They were joined by Dr Chuck Meakin, US Medical Director. It was truly inspiring for our doctors to hear that Yvonne continues to do very well clinically with ongoing stable disease, no new tumors in the liver and no sign of any suspicious lesions in other organs.

She also describes how the research and pursuit of additional evidence-led interventions, like the COC Protocol, has given her a mental and emotional boost, allowing her to exert positive influence over circumstances which, all too easily, can feel as though they’re outside a patient’s control.

At Care Oncology, we seek to empower our patients to help them live longer and better lives. But, we’re also with them every step of the way, providing ongoing medical supervision, regular follow up appointments with our doctors and access to nurse support. 

I am 29 and I have lung cancer – No, I do not smoke

I am 29 and I have lung cancer. And, before you ask: No, I do not smoke, have never smoked, and most certainly will NEVER start smoking so long as these sturdy lungs of mine can breathe. Cigarettes, as well as any of their close cousins [e.g. vape pens, e-cigarettes, cigars, or pretty much any object stuffed with injurious chemicals intended for bodily consumption], I have always found worth strenuously avoiding like the plague, or that irritable uncle of yours who corners you at family gatherings only to lecture you on society’s innumerable shortcomings, or the regrettable state of our politics, or the lackluster quality of today’s music, or…well, you get the point. You’ll have to forgive the acerbity, dear reader, as the general public – perhaps, even you – have succumbed to a dreadful misconception about me and others suffering from this horrible affliction. Remember this: You need not have smoked to get lung cancer, and that is a truth even the mighty gods of Olympus cannot impugn. Exposure to radon gas, air pollution, second-hand smoke, and, if recent research is to be believed, even third-hand smoke, are just some of the ways you can get lung cancer. More infuriating still, smoking is the leading preventable cause of most cancers[1] in the United States; however, when some unfortunate sap gets hit with a bladder cancer diagnosis, this is usually met with unhurried expressions of sympathy rather than, as is the case with lung cancer patients, an on-the-spot examination of the troubled victim’s [ugh, do I hate that word!] “history” of smoking.

You may be surprised by this. Appalled, even. Don’t be. It’s happened more times than I care to recount. Now, you’re probably wondering how someone like me – a healthy, physically active [I’m an avid runner], 29-year-old never-smoker – got lung cancer, right? Beats me. What you may not know is that in most patients with a similar profile [young, healthy, never-smoker], lung cancer is often discovered at a more advanced stage, when treatment options are few-and-far between compared to when the disease is caught at an earlier stage. In my case, I was completely asymptomatic. I had no difficulty breathing, my organs were functioning as they should, and I felt no discomfort whatsoever. My primary care physician even once joked during a follow-up appointment to discuss the results of my annual physical that I was “medically boring.” [Well, doc, you should see me now!] Until, of course, that fateful day in June of last year when I felt the left side of my body seize up while walking back to my office at work. I was later to discover that the cause of this seizure was an acorn-sized tumor that had metastasized to my brain from the primary tumor site in my right lung. You could imagine my surprise when I was given my diagnosis. Time immediately stood still in that moment. Like raging river waters that had broken through a dam, thoughts came flooding in: How did this happen? Where do I go from here? Could I have done anything to prevent this? And, most disturbingly of all, did I do anything to DESERVE this?

Prevention. We know the most effective way to treat patients is to not have to treat them at all. Despite some of my friends’ and family’s’ smoking habits, I never took up smoking and knew I never would. I ate right, barring the occasional late-night excursion to Taco Bell, exercised regularly (I still do), and did all I could to maintain my “medically boring” reputation. Sadly, it appears, that making all the right moves in life does not always guarantee you’ll come out on top. Luck, sometimes, plays an even greater role in the affairs of our species more than we care to admit. Let my story serve as a prickly and uncomfortable reminder of that fact.

You may be further tempted to ask: Could I have done anything to catch this disease at an earlier, more manageable stage? If only. What’s unfortunate is that, given my medical profile, the tests presently available to screen for lung cancer in patients for preventative or early treatment purposes would not have been available to me. Why? Well, among the eligibility criteria governing which patients are considered “high-risk” and should have annual low-dose CT screenings, the American Cancer Society lists the following: (1) persons  “aged 55 to 74 years and in fairly good health,” (2) persons who “currently smoke or have quit within the past 15 years,” and (3) persons who “have at least a 30-pack-year smoking history.”[2] Strike 1. Strike 2. Strike 3. I’M OUT! What about an X-ray, you ask? Not quite as effective as a CT scan. Not to mention, when I was hospitalized in June of last year, an X-ray of my chest was done, and this revealed absolutely nothing; the tumor was not quite large or dense enough for it to be picked up by the machine. And, though liquid blood biopsies are a novel and promising new screening mechanism employed by oncologists today to detect early signs of cancer, I would still have not been eligible to receive such testing for the same reasons that excluded me from receiving a low-dose CT screening; namely, I wasn’t considered “high-risk.” And that, to use the language of my gambling cohorts, is what we would call, a wash. Or, as my Francophilic friends would hurry to proclaim, C’est la vie.

However, I do not want to give you the wrong impression, dear reader. I’m not writing you in order to elicit your sympathy or pity. The world has no shortage of stories like mine, and I count myself not as possessing any special status far and above theirs. Though engendering a world in which love, kindness, and mutual understanding become ever more ubiquitous is a noble goal worth pursuing, my more immediate aim is simply to bridge what I and countless others see as a glaring gap in our public consciousness about lung cancer – its causes, its prevalence, and its victims. I bet you didn’t know that lung cancer is the LEADING cancer-killer in the United States, did you? Also, I can guess with near-to-absolute certainty that you didn’t know lung cancer kills MORE WOMEN every year than breast, uterine and ovarian cancer COMBINED. In fact, it is fairly evident lung cancer has no sex-specific predilections when it comes to choosing its victims, killing more men and women than any other cancer in the United States. I suppose, then, that in light of these findings, you’d be surprised (aghast, perhaps) to hear that lung cancer research garners the FEWEST dollars every year than any other cancer research initiative does? I can just picture you now, sitting there with furrowed brow, ponderously searching for an explanation that would account for such a depressingly large funding disparity. It’s quite simple, really: Lung cancer patients are seen as “deserving” their fate because they knew the risks when they began smoking. Of course, you need not be a master logician to see just how patently absurd this belief is. However, since I absolutely relish tearing apart fallacious arguments (my B.A. is in philosophy, after all), I would humbly ask that you allow me this one indulgence.

First, as was already made clear at the beginning, you need not have smoked to get lung cancer. In fact, as the rate of smoking continues to decline, a greater proportion of newly diagnosed lung cancer patients are younger, healthy, never-smokers like me. To edify you further: 60-65% of all newly diagnosed lung cancer cases are amongst people who have never smoked or who quit smoking some time ago. Estimated 10-15% of newly diagnosed lung cancer cases are amongst never-smokers. Sadly, however, the smoking stigma persists, and it is this stigma that needs quashing – and fast.

Secondly, let us dispense with the morally confused and abhorrent belief that anyone “deserves” cancer. Cancer patients are human beings, many of them with families and friends whom they hold dear, and who harbor dreams, goals, and aspirations much like your own. On all accounts, they are neither less nor more human than you are. It smacks as the height of arrogance to believe that any one mortal can sit in judgment of another, consigning them to a fate not of their own willful choosing. And, yes, while those who chose to smoke knew the risks they were assuming, it is also crucial to try to understand the prevailing contextual factors that would explain why such a deleterious habit was adopted to begin with. Passing judgment against those whose lives we may not fully understand makes us into moral monsters, not paragons of virtue. Furthermore, can any morally serious person believe that a mistake, once made, forever forecloses any opportunity for personal redemption? Indeed, is it not this opportunity for redemption that is the sine qua non of the virtue of forgiveness? By the way, you need not be of the religious variety to believe in the power of forgiveness. I, myself, am not particularly religious, though I do harbor spiritual beliefs of my own over which no religious organization or tradition can claim an exclusive monopoly. In short, if we cannot presume to know in their entirety the circumstances that would explain people’s poor past decision-making, it would be just as presumptuous of us to think that we can divine a person’s future chances at redemption or self-transformation. To think otherwise surely taxes the credulity of the credulous, and any person who feigns such omniscience should be treated with the scorn and ridicule that such claims rightfully deserve.

With that said, I suppose you have fully anticipated the crucially important point at which I’ve been driving with these (hopefully) thought-provoking moral queries and observations. If not, permit me to spell it out for you in language both unambiguous and emphatic: If we cannot justifiably rob one of our fellow mortal brethren of the chance to right past wrongs, to seek forgiveness (and, by extension, redemption), or to simply improve upon who they were in the hopes of achieving the best version of themselves, which is indisputably the object of all of our life’s exertions, then why should we allow cancer to do so? Let us not be so quick to heed the Siren call of fatalism, tempting though it be. The fatalistic attitude, which dismisses as un-malleable the circumstances of human existence, is something we must forcefully repudiate, and not just because it traffics in fabrications, but because it is crippling to the human spirit – a spirit that has made possible so many brilliant, innovative, and important achievements our species can lay claim to. If our species is ever to claim victory against such a historically cunning and formidable foe as cancer, than we must not let this spirit wane. To do otherwise would be to admit defeat, and defeat is most certainly not an option.

Ok, enough moralizing, lest I dissuade you from engaging in that introspection, which, I hope, my own ruminations put to paper on the topic of my own diagnosis provoke in you. If I have failed in that – if I have not sufficiently convinced you of the undeniable importance of self-reflection and the critical need to challenge unremittingly your underlying preconceptions, presuppositions, and prejudices – than, I’m afraid, people like me will continue to suffer needlessly under an unforgiving and confused stigma. Nevertheless, I have hope that, as Abraham Lincoln put it so poetically during his legendary address to those assembled at Gettysburg in 1863, that the “better angels of our nature” will prevail in the end.   

In truth, I take immense comfort in knowing that it is the untrammeled innovativeness of our species, together with our ability to remain hopeful during the darkest and bleakest of times, that will lead us with meteoric propulsion towards a cure for cancer of all types. Indeed, I do not think it exaggerated to claim that there has never been a better time to have cancer – heaven forbid you should get it. And this is not simply because of the promising new developments in conventional treatment options that we hear touted by the medical industry. No. We are at the beginning of a new epoch in the way cancer is understood; specifically, with respect to what causes it, and, thus, how it can be more effectually prevented and treated. Thanks to the unflagging efforts of pioneering medical professionals like Dr. Thomas Siegfried and Dr. Jason Fung (just to name two working professionals on a very long roster of professionals) and fastidious investigative journalists like Travis Christofferson, we have come to understand that our previous conceptualization of cancer as a genetic – or exclusively genetic – disease is woefully, indeed, fatally misguided.

In fact, as Dr. Siegfried and others have argued, cancer is a disease caused by a disruption in the normal metabolic functioning of our cells, and the genetic mutations conventional practitioners make haste in detecting are simply the effects (not the cause of) such metabolic dysfunction. New evidence continues to be amassed in support of this hypothesis, while pre-existing evidence thought to support the conventionally embraced genetic causal theory of cancer has been shown to be more supportive of the metabolic causal theory of cancer. As Dr. Siegfried and others have pointed out, when hundreds, if not thousands, of several different mutations can occur in even one solid tumor, focusing all our efforts on developing tailor-made therapies that may be able to target one of those mutations, and for a limited period of time, is to make poor use of what few resources and limited time we have in combatting this nefariously wily enemy we call cancer. If the metabolic theory of cancer has any credence – and I believe that it does – than a re-calibration of how we spend our precious time and resources when it comes to fighting cancer is in order.

For example, it may strike you as a surprise to discover that there is evidence to suggest that several re-purposed medications, such as the anti-diabetic drug Metformin, have anti-carcinogenic properties. These repurposed drugs are extremely mild in their toxicity, and are far cheaper to obtain than several conventional chemotherapeutic drugs (but don’t tell BigPharma I said that). It is pathbreaking discoveries, or, in some cases, re-discoveries like these that have been made by organizations, such as my virtual oncology platform, that are providing cancer patients with a newfound sense of hope where none may have previously existed. Additionally, other unconventional, but no less effective, therapies, such as high-dose IV vitamin C, have been shown to yield great promise as either monotherapies or adjunctive therapies[3].

Furthermore, simple changes to our dietary and eating habits – from the elimination of processed foods and sugar, to increasing our consumption of healthy alternatives, together with time-restricted eating or intermittent fasting and regular exercise – can all serve as effective weapons that you can store in your cancer-fighting arsenal. Uncovering all these latest developments in cancer research, I can honestly say, can be attributed to my voracious appetite for new information and unchecked intellectual curiosity – or, more simply put, to my inability, as my mother would say, to “sit still.” Those have always been two of my greatest assets, but they are assets, I believe, every cancer patient will need should they want to defeat this most cunning and devious of foes.

In some form or another, I have adopted the therapies, prescriptions, and practices mentioned above in my own life, as well as several more the details of which I will spare you (for now). However, I believe I would be remiss if I did not impress upon you the incalculable importance of supporting and maintaining a happy mental life, whether you have cancer or are seeking to keep it at bay (especially, if you’re trying to keep it away). Indeed, I believe that my failure to grasp this fundamental importance contributed, in one way or another, to my getting cancer.  As the influential philosopher Sam Harris once remarked, our minds are all we have, and that is undoutedly true. Though our understanding of the nature of consciousness leaves much to be desired, it is clear on virtually every account that our physical life is largely an extension of our mental life. More precisely put, our physical life is conditioned by our mental life, as the famed epigeneticist Bruce Lipton reminds us in his wonderful book entitled “The Biology of Belief: Unleashing the Power of Consciousness, Matter, and Miracles.”

To bring the point squarely into focus: A happy life suggests a mind that is unburdened of needless complications, indecision, stress, anxiety, and confusion, and can think about and comprehend things lucidly. Unfortunately, much about our contemporary lifestyles makes it all but impossible to cultivate a happy mental life. Social media sites vie for our uninterrupted attention, even as they contribute to the shortening of our individual and collective attention spans. Cable news networks shower us incessantly with one “news alert” after another, with each new alert more terribly inconsequential than the one that preceded it. And advertisers bombard us relentlessly with suggestions that we should all purchase the latest cellphone, luxury vehicle, or what-have-you in order to fill the void we feel deep inside us – a void, ironically enough, that is of the advertising industry’s very own self-serving creation. The stress induced by trying to “keep up with it all” is, I firmly believe, what is partly driving cancer to overtake heart disease as the leading cause of death on the planet. 

That is why I’ve decided to cut myself loose from these harmful distractions, and it’s why I think you should do so as well. Instead of feverishly checking your Twitter feed for the latest musings of a famous know-nothing, crack open a book on a subject you find interesting. I’m currently reading a brilliant biography on one of my favorite philosophers, David Hume. Unlike mindlessly scrolling through my social media feed, with the turn of each page, my mind does not suffer from diminishing returns. Rather than watching your politically-preferred cable news network of-choice, turn off that television and use that time to find a quiet place to meditate – to placate your mind, not to agitate it further with gratuitous noise, contrived conflict, and vacuous commentary. Lastly, find it in yourself to learn to love yourself. Without question, I’ve been characterized as somewhat of a perfectionist by those who know me best; however, in my drive to be the best, I was often my harshest critic. It was soon after I received my cancer diagnosis that I realized this was a terrible mistake. The biggest cause of the stress in my life came not from the outside, but from within.  I regret not realizing that earlier on. So, try not to be so hard on yourself. Perfection at the expense of finding that internal peace that makes for a happy life is too high a price to pay. So, refrain from paying it.

In conclusion, I would like to thank you for taking the time out of your busy (but, hopefully, not too busy) day to read my story. I hope it has aroused your curiosity and given you pause to reflect on some of those pre-conceived notions about cancer – especially, lung cancer – that you may have harbored prior to reading this article. Furthermore, I hope you use my story – improbable, though it may sound – to counter what are the altogether pernicious and prevalent misconceptions about lung cancer patients discussed earlier. Remember, if you have lungs, you can get lung cancer; it’s as simple as that, so consider a prevention strategy noted above. Now, before I dispatch with another one of my moralizing tirades and risk losing the progress I’ve made up until now, I’ll end it here. Go forth, and remember, that your personal well-being is the only thing of any real consequence in this life. And, in case you are wondering, I am thriving 18 months since that difficult day in June, and, for now, all is in remission. Rest assured; I intend to keep things that way.

With Love,


[1] “Cancers Linked to Tobacco Use Make up 40% of All Cancers Diagnosed in the United States.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 10 Nov. 2016,

[2] “Lung Cancer Screening Guidelines.” American Cancer Society,

[3] “A Combo of Fasting plus Vitamin C Is Effective for Hard-to-Treat Cancers, Study Shows.” ScienceDaily, ScienceDaily, 12 May 2020,

Future of Medicine Book “Curable” – EP09: Travis Christofferson (Author)

In this ninth episode, Travis Christofferson provides an overview of his new future of medicine book “Curable: How an Unlikely Group of Radical Innovators is Trying to Transform our Health Care System”. He covers the great inefficiencies of healthcare and harm it’s doing to swaths of the patient population. He explains it’s too qualitative than quantitative, that incentives are misaligned. He offers hope by urging a shift to being data-driven.


COC Comment: New Research on COC Medications and NSAIDs

A large South Korean registry study has shown that the combination of two COC Protocol medications (metformin & statin) alongside aspirin reduced lung cancer incidence and mortality. The study also indicated that the potential for benefit increased the longer the duration of use –

Summary here
Full paper here

This is interesting as:

a) it adds to the research literature which suggests the combination of metformin and statin may exert synergistic anticancer effects (see, for example, recent papers in the context of Prostate and Endometrial cancer. Click to read more

b) it bolsters existing evidence on the potential usefulness of NSAIDs such as aspirin and ibuprofen in a cancer context. Click to read more