Category: News

COC Protocol for Early Stage and Stable Disease

Historically, patients have often presented to Care Oncology physicians with advanced disease– either they have been diagnosed with a type of cancer associated with a particularly poor prognosis or they have suffered a recurrence/disease progression and feel their conventional treatment options are becoming more limited. 

However, there are good reasons to also consider the adjunctive COC Protocol if you are a patient with either an early stage cancer diagnosis or someone who is currently well with more advanced stage 3 or 4 disease. Indeed, the likelihood of a positive outcome is greater than with late-stage presentation.

First, a significant body of research literature suggests that using anti-metabolic drugs such as metformin and statins as adjunctive therapy to standard of care can enhance overall treatment response.

Second, in a scenario where the patient is well in him/herself and/or has a lighter burden of disease, there may be an even greater likelihood of effective disease control.

Our own cohort analysis of 95 patients with Glioblastoma IV (the most common and aggressive type of primary brain tumour in adults) supports this conclusion. These patients were all prescribed the COC protocol alongside their standard of care treatment. Median overall survival of the cohort as whole is considerably better than median overall survival with standard of care alone (  But, those patients who commenced the COC protocol during or soon after first line chemo-radiotherapy have a longer median overall survival than those coming to it after having suffered progression/recurrence. 

Importantly, in‘’well patients” with a good performance status, we would also expect to see better compliance with the COC protocol medicines and fewer side-effects and/or a requirement to interrupt or stop treatment as a result of abnormal blood counts or organ function. 

In addition to the work we are undertaking, a number of other studies are currently underway to explore reduced relapse in patients taking anti-metabolic medications, for example, the very large Cancer Research UK funded ADD-Aspirin trial enrolling 11,000 patients across 5 different types of cancer.

When a patient hears that they are well and perhaps ‘in remission’, they often assume that this means they are cured and are done with treatment. While the words‘remission’ and ‘no evidence of disease’ (NED) are clearly good news and can mark a major positive turning point in someone’s care and overall health,unfortunately, the true situation is often more complicated.

There is no way for doctors to know that all of the cancer cells in your body are gone, which is why many doctors don’t use the word “cured.” If cancer cells do come back, it usually happens within the 5 years following the first diagnosis and treatment. 5 year survival rates or survival statistics are available for all the different types of cancer seen in the community. These statistics are based on research from information gathered on hundreds or thousands of people with a specific cancer.

An overall survival rate includes people of all ages and health conditions who have been diagnosed with a specific cancer, including those diagnosed very early and those diagnosed very late.

Doctors are then often able to provide more detailed statistics based on the stage of cancer at diagnosis. For instance, 56% or a little more than half, of people diagnosed with early-stage lung cancer live for at least five years after diagnosis. The five-year survival rate for people diagnosed with late stage lung cancer that has spread (metastasised) to other areas of the body is 5%.

Because survival rates can’t tell you everything there is to know about your individual situation, the statistics may seem impersonal and unhelpful. But, many people feel that that knowing as much as possible about their cancer, actually helps them to reduce their anxiety, as they can then analyze the different options available to them.  

While, of course, it’s up to each individual patient to decide just how much they want to know about survival rates and overall prognosis, Care Oncology physicians believe the risk/benefit of metabolic adjunctive treatment to be in the patient’s favour if there is judged to be a significant risk of cancer progression or recurrence.

The COC protocol is:

  • Evidence-based; the weight of the available data demonstrates a significant opportunity for patient benefit. Some mechanisms which underpin the utility of the protocol drugs may be particularly helpful in a preventative setting e.g. inhibition of Cancer Stem Cells.
  • Low toxicity, generally well-tolerated and ‘easy to do’ (i.e. tablets, capsules to be taken at home).
  • An adjunctive therapy with a low drug interaction burden which can be incorporated alongside other lines of treatment
  • Almost always safe to combine with standard of care treatments (chemo-, radio-, hormone-, immuno-therapy)
  • Able to potentiate standard treatments by making cancer cells more sensitive to chemotherapy or radiotherapy than would otherwise be the case.

Click here for more information and research references

Click here to check your eligibility for the COC Protocol

FutureTechPodcast: Understanding and Treating Cancer: Epigenetics, Metabolic Therapy, and Repurposed Drugs

What’s the ultimate cause of cancer? Travis Christofferson is interviewed on the FutureTechPodcast.

It’s not an easy question to answer, and according to Travis Christofferson, author of Tripping Over the Truth: The Return of the Metabolic Theory of Cancer, there’s no single cause, but a series of complex interactions and events that depend at least somewhat on our environment. Christofferson explains this in terms of epigenetic responses, which result in the turning off or on of certain genes–allowing some to be expressed and blocking others from being expressed. Diet, toxins, medications, and even loneliness are just a few of the factors that could trigger epigenetic responses and ultimately contribute to the determination of whether or not someone will develop cancer.

Antioxidants and Cancer – Should I take them?

Our Care Oncology physicians often get asked their opinion on various supplement including common and uncommon antioxidants: vitamin C, vitamin E, beta-carotene, N-acetylcysteine (NAC), and glutathione to name a few. Understandably, newly-diagnosed cancer patients and their friends and family often embark on a deep search for anything that can be done to support health and immune system function. And why not antioxidants? A steady stream of media and supplement manufactures have told us for decades that antioxidants offer a panacea of health benefits. And rightfully so, a light internet search can easily lead to articles touting the virtues of antioxidants. The calculus: They may help fight my cancer, and, in the very least, they can’t hurt. Right?

Where did the idea antioxidants are good come from?

In 1972 Denham Harman, a luminary in the field of free radical biology, proposed the mitochondrial theory of ageing. It goes like this: Inside every cell mitochondria are the center of oxidative metabolism and hence the primary source of free radical generation within the body. Free radicals generated from mitochondria then precipitate a cascade of damage to surrounding mitochondria, lipids, carbohydrates and even nuclear DNA. The cell can repair most of this damage, but over time the cell slowly loses the ability to keep up with the free radical induced damage and the net damage that ensues is the proximal cause of ageing.

spoon with dietary supplements on fruits backgroundA simple and intuitively seductive assumption sprang forth from Harman’s theory: free-radical quenching antioxidants should slow ageing and prevent disease. This seemingly innocent prediction has confounded a generation of molecular biologists. In the over forty years that followed Harmon’s prediction researchers have shoved antioxidants into cell cultures, mice, rats, monkeys and humans trying to prove they slow ageing and prevent disease.

Despite their best efforts to prove otherwise, an overwhelming consensus has emerged from the decades of research on antioxidants and ageing: they just don’t work. They might correct dietary deficiencies and/or perhaps confer a slight protective effect against certain diseases, but they do nothing to prolong lifespan—worse, there is evidence to suggest they may even promote certain diseases. Yet, almost a half century of inertia and a billion-dollar supplement industry that grew out of Harmon’s prediction have managed to continue propping up the notion that antioxidants are a well-spring of health. (Don’t confuse foods containing antioxidants and antioxidant supplements. Most quality food contain high amounts of natural antioxidants and a good diet has been shown to be very beneficial.)

Studies began to challenge many assumptions about antioxidants

The blanket assumption that antioxidants slow ageing and prevent disease was first seriously challenged from a large study in 1994 that followed smokers taking massive doses of the antioxidant beta-carotene. The stunning result: The smokers taking beta-carotene had an 18% increased risk of developing lung cancer. As researchers were still scratched their heads about the confusing result a trial two years later was stopped early after it was discovered that high-dose beta carotene and retinol was shown to increase the risk of developing lung cancer by 28 percent in smokers and workers exposed to asbestos. And these early studies are not proving to be flukes: a 2011 trial involving more than 35,500 men over 50 found that large doses of vitamin E increased the risk of prostate cancer by 17 percent.

Antioxidants and cancer therapy

The above studies highlight a trend of studies suggesting that antioxidants may contribute to the incidence of certain cancers under specific conditions and may make cancer more aggressive when it occurs. However, the series of studies sparked a more immediate concern to practicing oncologists: because traditional standard of care therapies like radiation and chemotherapy kill cancer cells by the generation of free radicals perhaps patients taking antioxidants were negating or diminishing the effects of their cancer treatment. Yet, despite a flurry of studies in the early 2000’s―both observation and randomized controlled trials―no clear consensus of the effect of antioxidant on standard therapies emerged. The studies reached a wide variety of conclusions, some showing improved survival and status and others, a reduction in survival. Most likely, the common antioxidants, given at normal doses, are simply to weak to overcome the powerful effects of radiation and chemotherapy.

The smoldering debate about antioxidants and cancer was rekindled again in 2012 when Nobel Prize winner and former head of the NCI, James Watson, sounded off on the danger of antioxidants in cancer, penning a review titled Oxidants, antioxidants and the current incurability of metastatic cancers, claiming the work was “His most important work since the double helix.” His epiphany, in part, was the claim that antioxidants may be thwarting most cancer therapies if not outright causing cancer by preventing the mitochondrial driven apoptotic cascade triggered by free radicals. “For as long as I have been focused on the understanding and curing of cancer (I taught a course on Cancer at Harvard in the autumn of 1959), well-intentioned individuals have been consuming antioxidative nutritional supplements as cancer preventatives if not actual therapies. In light of the recent data strongly hinting that much of late-stage cancer’s untreatability may arise from its possession of too many antioxidants, the time has come to seriously ask whether antioxidant use much more likely causes than prevents cancer.” Watson goes on, “Free-radical-destroying antioxidative nutritional supplements may have caused more cancers than they have prevented.”

A series of studies in the years following Watson’s revelation seemed to support his claim. A 2015 study published in Science Translational Medicine, looked at melanoma because rates have been increasing and because the cancer is known to be sensitive to the effects of free radicals. They fed the antioxidant N-acetylcysteine (NAC) to mice that had been bred to be susceptible to melanoma at a dose consistent with what people typically consume in supplements. Although the treated mice did not develop more skin tumors than the control mice, they developed twice as many tumors in their lymph nodes, a hallmark of the spread of cancer. When the researchers added NAC or a form of vitamin E to cultured human melanoma cells, they again showed that the antioxidants improved the cells’ ability to migrate and invade a nearby membrane.

Additional evidence surfaced pointing to the danger of antioxidants new classes of free radical generating therapies. A study that came out immediately before Watson’s paper convincingly showed the importance of free radical induced apoptosis by the finding that the ‘first-in-class’ anti-cancer mitochondrial drug elesclomol kills cancer cells through promoting ROS generation. When these resulting free radicals were neutralized through the simultaneous administration of the antioxidant N-acetylcysteine, preferential killing of cancer cells stops. The failure of elesclomol to generate apoptosis in non-cancerous cells probably arises from the inherently lower ROS level generated by normal mitochondrial electron transport machinery.

Critically, many new therapies are being developed that lower the glutathione level in cancer cells rendering them more vulnerable—it is not clear how antioxidants will affect this new class of drugs and therapies.

The picture remains murky

Although there is no overwhelming consensus that antioxidants taken during cancer treatment will lead to worse outcomes the existing evidence throws up enough red flags to warrant caution. Not much is known about the effects of antioxidants in relation to many of the new metabolic-acting and immunotherapies. It must be considered that adjunctive therapies like the ketogenic diet, hyperbaric oxygen and the Care Oncology Protocol are also proposed to work by triggering oxidative stress in cancer cells while simultaneously reducing the cancer cells ability to manufacture internal antioxidants. It is not unreasonable to question the use of antioxidants concurrent with these therapies―especially considering they tend to generate much milder oxidative stress than tradition cancer therapies and therefore antioxidants might have the capacity to influence outcomes to a greater degree. In fact, evidence exists highlighting this tenuous relationship. It has been shown that some of the medications in the Care Oncology Protocol act by inducing oxidative stress within cancer cells. Both doxycycline and metformin are proposed to work by inducing an intolerable surge of free radicals within already oxidative-stressed cancer stem cells while simultaneously inhibiting a transcription factor called STAT3 that the cancer cell upregulates in order to manufacture internal, adaptive antioxidants—a sort of one-two punch. A 2017 study showed that the addition of the potent antioxidant N-acetylcysteine was able to cancel-out the therapeutic effect of doxycycline in a glioblastoma mouse model.

“What we’re starting to learn is that there can be bad cells from cancer that appear to benefit more from antioxidants than normal cells,” said researcher Sean Morrison from the University of Texas Southwestern Medical Center, who’s lab studies the effects of antioxidants on cancer cells. “Personally, from the results we’ve seen, I would avoid supplementing my diet with large amounts of antioxidants if I had cancer.”

Martin Bergö, Ph.D., of the University of Gothenburg in Sweden, said he was extremely concerned with the aggressive marketing of antioxidants to cancer patients. The data strongly suggest that using antioxidants “could be really dangerous in lung cancer and melanoma, and possibly other cancers,” he said. “And because there’s no strong evidence that antioxidants are beneficial, cancer patients should be encouraged to avoid supplements after they have a diagnosis.”

Care Oncology Science Advisor, Thomas Seyfried of Boston College shares Morrison’s and Bergö’s sediment. “Why would you give antioxidants to cancer patients? It runs completely counter to metabolic therapeutic interventions.”

Indeed, the general idea that oxidative stress might be one of cancer’s greatest vulnerabilities, and that antioxidants, both exogenous (taken orally or by IV) and endogenous (manufactured intracellularly), may represent a thin veil of protection that can be therapeutically targeted is also proving to hold true with the emerging class of immunotherapies. New research has shown that by reducing intracellular glutathione, the cell’s “master antioxidant”, the cell-killing effect of immunotherapies can be enhanced. The authors of the recent study state: “The inhibitory effects of cancer on T cell metabolism have been well established, but the metabolic impact of immunotherapy on tumor cells is poorly understood. Here, we developed a CD4+ T cell-based adoptive immunotherapy protocol that was curative for mice with implanted colorectal tumors. By conducting metabolic profiling on tumors, we show that adoptive immunotherapy profoundly altered tumor metabolism, resulting in glutathione depletion and accumulation of reactive oxygen species (ROS) in tumor cells.”

Well what now?

In the over forty years since Harman’s proposed free-radical driven mitochondrial theory of ageing we’ve learned that free radical biology is certainly more complex than originally appreciated. While there is no question free radicals are destructive to the cell, emerging evidence suggests mitochondrial derived free radicals may also be an important signaling system, instructing the DNA within the mitochondria to manufacture mitochondrial proteins. Free radical biology and its ultimate role in ageing is still unsettled science that has yet to be conclusively decided.

However, the relationship of antioxidants and cancer, although still murky, seems to be tilting toward a note of caution when it comes to including antioxidants as part of cancer therapy. While little if any benefit has ever been proven, the evidence pointing against their use does demand attention. A cautious approach would be to avoid high doses of antioxidants during cancer treatment. A very cautious approach would be to avoid antioxidant supplements altogether. Indeed, most dieticians agree that enough micronutrients can be obtained―and in the right ratios―from a good diet.

Some common antioxidants:

Vitamin E, selenium, zinc, N-acetylcysteine, glutathione, Vitamin C (low dose only—high doses administered by IV are oxidative), and beta-carotene


Check your eligibility for the COC Protocol now by filling out the following form:

Research shows that drugs found in the COC Protocol have an antiproliferative effect on breast cancer tumor cells, meaning that the drug inhibits the growth and spread of cancer cells.

How will the COC Protocol help treat breast cancer?

The COC protocol is a patented pharmaceutical composition of four repositioned medications. The medications have long histories treating type-2 diabetes, reducing cholesterol, parasite infection, bacterial infection and inflammation. After four years of clinical research, we know that these drugs – in combination – offer significant therapeutic value for cancer patients. Each of these drugs plays a role in weakening cancer cells and making them more susceptible to standard-of-care therapy (e.g., chemotherapy, immunotherapy).

One of the biggest problems breast cancer patients face is when their cancer becomes resistant to standard-of-care therapies. Multi-drug resistance (MDR) occurs when a patient develops resistance to one or more treatment drugs.

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Can a diabetes drug control Pancreatic Cancer?

The study — which was led by Rutgers Cancer Institute of New Jersey in New Brunswick — is to feature at the 2018 annual meeting of the American Association for Cancer Research, which will be held in Chicago, IL.

This study is not the first to suggest metformin as a potential treatment for pancreatic cancer, but it is the first to show that the underlying mechanism involves the drug’s effect on the REarranged during Transfection (RET) cell signaling pathway.

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You’ve got to believe you can beat it – Kent R. – Grade 4 Glioblastoma Patient

Glioblastoma Patient Interview – COC Treatment Protocol

Kent: Hi, my name’s Kent Rhodes and I have a Grade 4 Glioblastoma, and I was first diagnosed on the 27th of September 2016. After the initial, I suppose shock would be a good word, I visited Care Oncology on the 14th of October 2016, and met the wonderful Ndaba who told me how we were going to save my life. And the rest, as they say, is history. At the moment we are doing very well.

Ndaba: Well, thank you very much, Kent. What led you to seek additional options for treatment?0

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I am an active, 48 year old mother and wife, and I am not ready to leave my family and friends. – Glioblastoma Diagnosis

After my devastating diagnosis of Glioblastoma Multiforme, an aggressive and deadly form of brain cancer, I was told that the standard of care treatment would give me a 3% survival rate with a possibility of living for 12-15 months.

I am an active, 48 year old mother and wife, and I am not ready to leave my family and friends. I needed to find some alternative treatments because the standard medical ones were insufficient.

In my frantic and non-stop research, I repeatedly found and read about Care Oncology’s research and findings. Not until a friend in London, who happens to be in the medical field, advised me to do so, did I visit Care Oncology’s website and delve further into COC’s protocol. I was intrigued by their evidence-based approach. As I researched further, I found that the COC’s treatment was having success and garnering accolades from the research and medical community. I wanted to be part of their protocol.

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The COC Protocol – Featured in Daily Mail – Henry was given 14 months to live now his cancer is stable

We tend to associate breakthrough treatments with new — and often unaffordable — drugs.

But it seems a remarkable improvement in the survival time of patients with brain cancer has been achieved using a combination of four old drugs (a statin, a diabetes pill, an antibiotic tablet and a dewormer) that cost just £400 a year.

Results from an ongoing trial run by the private Care Oncology Clinic in London suggest that giving this new combination treatment doubled the average survival time.

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Widely Prescribed Oral Diabetes Drug Leads to Dramatic Breakthrough Cancer Treatment

Although rare, adrenocortical carcinoma is among the most common tumors found in children with Li-Fraumeni syndrome and Li-Fraumeni-like syndrome, associated with germ-line mutations in the TP53 gene. In southern Brazil, one form of Li-Fraumeni syndrome, associated with childhood adrenocortical carcinoma, is caused by a mutation in the R337H TP53 tetramerisation domain and is attributed to a familial founder effect. Adrenocortical carcinoma is considered an aggressive neoplasm, usually of poor prognosis and is generally unresponsive to systemic chemotherapy. Optimal treatment regimens remain to be established. We report the case of a young woman with metastatic adrenocortical carcinoma, who achieved stable disease with mitotane, cisplatin, doxorubicin, and etoposide as first-line therapy, but then had an objective response to oral metformin that lasted 9 months. The presence of the R337H TP53 mutation suggests a mechanism for the observed response to metformin.

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The question is – why wait to add in the COC drugs to your cancer treatment when it may potentially help whilst doing very little harm?

Patient Testimonial – 40 year old female with breast cancer

1) When did you first visit Care Oncology Clinic and commence adjunct treatment? What led you to seek out additional treatment options?

I first visited the COC in September 2016. This was halfway through my chemotherapy treatment for breast cancer.

Despite the intended outcome of my primary cancer treatment to be curative, I was shocked by the number of women I met through support groups who had experienced a return or spread of their breast cancer in the years after completing primary treatment. I then analysed the statistics and profile of my cancer diagnosis – it suggested I also faced this risk. I simply knew I had to do more.

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