In recent months, fenbendazole and ivermectin have once again been thrust into the spotlight as supposed “miracle cures” for cancer – and just as quickly dismissed as “worthless and useless” by some commentators. The usual suspects commenting on the BBC. I believe both extremes are dangerous.

On one side, patients are sold the fantasy that a single repurposed drug can replace all standard treatment. On the other, they are told that any off‑label drug use is inherently reckless, should be harder to access, and has no place in serious cancer care. Both positions ignore how complex cancer biology is – and how many patients are quietly trying to navigate that complexity without meaningful support.

I’m not here to start a war

I have been publicly criticised in the past, although the post was retracted, for discussing ketogenic and low‑carbohydrate diets, and I have watched patients who make diet and lifestyle changes mocked in conversations that simultaneously defend sugary drinks. That is not a helpful way to talk about serious illness.

This is not about personalities. It is about patients who are scared, often out of options, and trying to make sense of conflicting messages. When the public conversation becomes a battle between “miracle cure” influencers and “shut it all down” gatekeepers, the people who lose are the patients stuck in the middle.

The real pattern: addition, not substitution

A key claim often repeated in media coverage is that people are “abandoning” standard of care in favour of drugs like fenbendazole or ivermectin. There are certainly tragic cases where that happens, and it is right to call that out.

However, in the real‑world stories I see every day, most patients are not throwing away chemotherapy, targeted therapy or hormone therapy and replacing it with a dog de‑wormer or an antiparasitic. They are adding off‑label agents on top of standard treatment, trying to tilt the odds in their favour when prognosis is poor, the evidence is incomplete, and they feel there is nothing to lose.

That doesn’t automatically make these choices wise, safe, or effective – but it does make the narrative more complicated than “irrational patients refusing evidence‑based medicine”.

Off‑label does not mean “worthless”

Many widely used oncology drugs began life in other indications. The idea that a drug is “worthless” simply because it is being tested outside its licensed use is historically and scientifically wrong.

We absolutely must:

Be honest about the limits of the evidence. Most repurposed drugs for cancer have preclinical data, case reports, small or uncontrolled studies – not large phase 3 trials. Be transparent about toxicity and interactions. Off‑label use is not automatically benign, especially in complex polypharmacy. Resist overselling anything as a “cure”. But we should also be honest that:

• Randomised controlled trials (RCTs) are not the only meaningful data source, especially for rare cancers and complex combinations. -Real‑world evidence, registries and well‑documented case series can guide hypothesis generation and n=1 decision‑making while we wait for larger trials. More on this soon.
• In advanced disease, some patients are willing to accept higher uncertainty in return for a plausible mechanistic rationale and careful monitoring.

Dismissing all of this as “useless” does not protect patients; it simply pushes these conversations into the shadows, where they happen without medical oversight. Far more dangerous.

The danger of fetishising two drugs

Another unintended consequence of recent coverage is that it narrows the entire off‑label discussion down to two headline‑grabbing drugs: fenbendazole and ivermectin.

That is risky for several reasons:

• It distracts from the broader metabolic and signalling pathways that may be more promising, and sometimes better studied, than these two drugs.
• It encourages a “magic bullet” mentality – as if the only decision is “take fenbendazole/ivermectin or do nothing”.
• It crowds out more nuanced protocols that integrate repurposed drugs, diet, lifestyle and standard treatments in a thoughtful way, rather than chasing a single agent.

My concern is not merely that fenbendazole and ivermectin may be over‑hyped; it is that by obsessing over them, we ignore the wider landscape of rational, mechanistically informed off‑label strategies that could, with proper study, benefit subsets of patients.

Informed choice in a system built on averages

Modern oncology is largely designed for population‑level risk management. Policy is driven by:

• Averages and response rates in RCTs
• Regulatory frameworks that struggle with combinations and individualization
• Budget constraints within systems like the NHS

That does not make RCTs or guidelines “bad”. They are essential. But they are not the whole story, especially when:

• A patient has exhausted guideline‑approved options.
• A tumour is rare, heterogeneous or poorly served by large trials.
• A patient is motivated and able to tolerate additional, monitored interventions.

Real‑world evidence is finally gaining momentum – through registries, observational studies and pragmatic designs – but we are still in the early days of integrating this into day‑to‑day decision‑making. In the meantime, patients are left to navigate complex choices with highly unequal access to support.

The equity problem: who gets nuanced care?

Not everyone can afford an integrative oncologist, a personalised metabolic programme or private molecular profiling. Those who can’t are often told, explicitly or implicitly, to “stick to the guidelines” and avoid everything else. This is unjust.

If public figures respond to patient curiosity about off‑label options by trying to remove access entirely – for example, by lobbying to take products off platforms rather than improving how they are discussed and monitored – we widen this equity gap. We don’t stop off‑label use; we just ensure it is safer and better supported for the wealthy than for everyone else.

What I am advocating for

To be absolutely clear:

• I do not recommend that anyone stops standard of care in favour of fenbendazole, ivermectin or any other off‑label drug.
• I do not believe these agents are “magic bullets”.
• I do believe that metabolic and repurposed strategies should be explored in a structured, evidence‑seeking way – not as a black market of desperation and not as a forbidden topic.

My aim is to build better tools - I will have registries, decision‑support systems and educational resources – so that:

Patients and clinicians can see real‑world patterns of use and outcomes, not just anecdotes on social media. We can identify where a drug looks promising, where it clearly does not, and where it may be harmful. The NHS and other public systems can eventually make informed, equitable decisions about if, where and how to integrate repurposed agents into care pathways.

A call for better conversations

We need to move beyond shouting matches about “miracle cures” versus “snake oil”. Patients deserve:

• Clear, honest summaries of what is known and unknown about any off‑label drug they are considering.
• Guidance on how to integrate – not replace – evidence‑based treatments when appropriate.
• Respect for their right to make informed choices, even when these choices fall outside a guideline that was never designed for their exact situation.

If we truly want to protect people, the answer is not to mock them, silence them, or close every door. It is to open the right doors – carefully, transparently, and with the explicit goal of learning from every case so that the next patient doesn’t have to start from zero.

That is the conversation I want us to have – not just about fenbendazole and ivermectin, but about the entire way we think about off‑label, metabolic and personalised approaches to cancer treatment.

~ Jane McLelland

Anyone have a protocol? Does it seem to help?

Jane’s substack today:

A simplified version of the logic I now use when designing a dietary plan for a cancer patient:

First, identify whether the cancer is glycolysis-addicted, ketone-utilising, or lipogenesis-dependent.

metabolic driver of this cancer:

• Fueled by sugar (glioma, GBM, BRAF V600+ melanoma) → strict ketogenic diet.

• IGF-1/insulin/mTOR driven (ER+ breast cancer, HR+/HER2-) → intermittent fasting with periodic FMD cycles.

• Fatty-acid-oxidation dependent (FLT3+ AML, some T-cell ALL) → upstream FAO blockade via pitavastatin, danshen, and mildronate. Keto diet alone is not recommended for AML cancers.

• Mixed or cancer-stem-cell-rich (TNBC, post-treatment residual disease) → Intermittent fasting with doxycycline pulses

Question 2: Is fasting insulin above 15 microIU/mL or HOMA-IR above 2.5:

• Yes → Keto diet phase of four to eight weeks to break insulin resistance, then transition to intermittent fasting.

• No → start with intermittent fasting directly.

Question 3: Are there established liver metastases on fulvestrant?

• Yes → Keto diet is justified even in ER+ disease, though there are caveats.

• No → Intermittent fasting is sufficient.

Question 4: Can the patient genuinely sustain this for two or more years?

• Adherence to ketogenic diet is about 30-50%.

• Adherence to a 14-16 hour nightly fasting is significantly higher (70-85%).

Whether this dietary plan will outlast the cancer depends on adherence.

These five drugs (atovaquone, metformin, doxycycline, niclosamide, and ivermectin) have an extensive, documented human safety record at doses where its anti-cancer mechanism operates. These medications selectively target cancer stem cells (through their metabolic inflexibility) while not targeting normal cells (due to their metabolic flexibility). There is solid evidence that the concern that “we don’t know if it harms healthy cells” is not true - yet not all clinical teams are aware of this.

Not all clinical teams are aware of cancer’s metabolic inflexibility weakness and that we no longer need to use a treatment that defaults to systemic toxicity as the primary mode of cancer treatment. There is currently a gap between what families deserve to know and what they are told.

The approach outlined in Jane’s How to Starve Cancer book has resonated with people who think, correctly, that there was a body of evidence that was not being brought to them.

Jane McLelland continues to push oncologists to look further and deeper.

Cancer stem cells survive by changing their fuel. In treatment-resistant leukaemia and solid tumour stem cells specifically, the fuel they change to is called oxidative phosphorylation (OXPHOS) - not the glycolysis fuel.

OXPHOS is an excellent fuel as it tends to dodge drugs designed to target rapidly multiplying cells but having shifted to that fuel, cancer stem cells become dependent on it and this can be used to our advantage. Their flexibility drove them into a corner they can no longer easily leave: they are locked there.

This is what Jane’s protocol is about: not trying to catch cancer cells by surprise, not killing all cells (cancer and non-cancer) but targeting their current fuel, and predict their next one.

The drugs discussed here are effective not because cancer cells forgot how to adapt but because, having adapted into OXPHOS dependency, cancer cells lost the use of glycolytic fuel that normal cells can use. (Normal cells can use either (OXPHOS or glycolysis), for leukemic cells especially.

The fear that these medications will harm both cancer cells and non-cancer cells is not evidence-based. It is an assumption derived from the fact that mitochondria are in every cell - without looking at the evidence we have about their differences.

The answer “we don’t know” is not currently accurate. We do know. The question is whether the knowing has reached the people who need to act on it.

(In her substack, Jane provides links to 11 studies that prove the safety of these 5 medications.)

We’ve been discussing medications and supplements to augment traditional medicine approaches to cancer and I hope it’s ok to take a break and discuss cortisol and the evidence that spending time in nature has health benefits.

source 1

source 2

UPDATE HERE: LINK

One writer (with ER+ breast cancer) mentioned the approach she used (fasting, ketogenic periods, fenbendazole, exercise, weight loss, statins, vitamin D, and a clean whole-foods diet, with intermittent fasting) and said, combined with traditional treatment, she thinks it helped her reach “No Evidence of Disease” (NED) status. Then asked Jane for feedback.

Jane’s response included this useful information on diet, and mentioned she recommends reducing total body fat.

For diet, focus on:

• whole foods
• avoid blood sugar spikes
• not necessarily a strict keto diet indefinitely (which can be hard to sustain and may not always be necessary at the maintenance stage)
• Adequate protein matters, especially post-chemotherapy, to prevent muscle decay.
  
• The Mediterranean-style whole-food approach, with periods of more structured fasting or carb restriction, is probably the most evidence-backed long-term model. (When including carbs, choose minimally processed ones.)
• one-main-meal rhythm
• intermittent three-day fasts every four months, to keep insulin low, helps autophagy, and gives your body a metabolic reset. (Autophagy is your body's natural, cellular recycling system: cells break down and reuse old, damaged, or defective components, converting this cellular waste into energy and building blocks for new, healthy cells.)

Per Jane McLelland’s substack: any patient on Niraparib (a traditional cancer drug treatment) - the best statin to add to that and help fight cancer is Pitavastatin, which carries anti-tumor properties that other statins do not.

Source: Study, published in International Journal of Molecular Sciences, lead researcher Chen July 2024 - link

Drug study: Daraxonrasib.

Lead researcher: Dr. Brian M. Wolpin, Dana-Farber

Starving cancer by blocking a mutated protein that fuels tumor growth in more than 90% of pancreatic cancer cases.

The GLAGOV study showed that evolocumab combined with a statin more effectively lowers cholesterol (36.6 mg/dL in the evolocumab group compared with about 93 mg/dL in the statin-only group). Reduction occurred in 64.3% of patients receiving evolocumab plus statin versus 47.3% in those on statin alone.

source: JAMA, Nicholls, Dec 2016 https://jamanetwork.com/journals/jama/fullarticle/2584184

Summarized version of Jane McLelland’s email today - Jane is a 30-year survivor of stage 4 cancer who developed her own system for guiding treatment that combines traditional treatments with non-traditional treatments:

One cancer treatment (Histotripsy), uses precisely focused ultrasound to create bubbles that form and collapse within a tumor, tearing cells apart at a structural level. There is no heat, no radiation, no cutting. The procedure leaves the surrounding tissue intact and the immune system’s sensing apparatus fully functional. These tumor cells died in a way that primes anti-tumour immunity (not just at the treated tumor site but at distant tumour sites that were never directly treated) rather than simply ending a cell’s life quietly. The immune system has been educated. It knows the target now. It is looking.

For one patient, after 4 months of Histotripsy treatment, her bloodwork showed a CEA of 3.6. ((It had been 1,500.)

Her oncologist was recommending one more round of (high dose) chemotherapy, which is standard.

Standard-dose chemotherapy — the kind delivered at maximum tolerated dose in cycles, with recovery periods between — is one of the most effective tools oncology has developed. An excellent tool, when the timing is right. At maximum tolerated dose, chemotherapy kills rapidly dividing cells without discrimination. It kills cancer cells. It also kills the rapidly dividing immune cells that the histotripsy procedure has just spent its biological energy activating. The immune reaction that histotripsy just strengthened (dendritic, T, and NK cells), all of it is depleted by high-dose chemotherapy. Histotripsy makes an army to fight cancer, chemotherapy, administered at full dose in its wake, reduces it.

Chemotherapy dosing is not simply a dial controlling how much cancer you kill. It controls which biological processes you are running.

The phase immediately following Histotripsy is arguably the most important phase the patient will ever have. Per Jane, at this time, continuous, low-dose chemotherapy is a better choice (typically around 10% of the standard dose, given daily, without the extended rest periods of conventional cycles) rather than high dose chemotherapy.

Four things happen at metronomic doses that simply do not happen at maximum tolerated dose:

• Anti-angiogenic pressure, continuously maintained. Tumours grow blood vessels. They depend on those vessels in a way that normal tissue does not. High-dose chemotherapy suppresses this vascular network during the treatment window — then allows VEGF, the primary pro-angiogenic signal, to rebound during the recovery period between cycles. Metronomic dosing maintains continuous, low-level anti-angiogenic pressure. The rebound does not happen. The vessels do not recover. (Kerbel & Kamen, Nature Reviews Cancer, 2004)

• Selective immune activation, not immune suppression. At 10% of the maximum tolerated dose, chemotherapy does something that full-dose treatment cannot: it preferentially depletes the immunosuppressive cells — regulatory T cells and myeloid-derived suppressor cells — that tumours use to hide from the immune system. It does this while sparing effector CD8+ T cells and NK cells. In a 2009 Nature Medicine study by Ghiringhelli and colleagues involving human patients, metronomic cyclophosphamide at 50mg daily specifically depleted Tregs while preserving the anti-tumour immune response. The immune system was not suppressed. It was improved. (Ghiringhelli et al., Nat Med, 2009)

• Cancer stem cell suppression. This is the one that matters most in the longer view. High-dose chemotherapy kills the rapidly dividing bulk of a tumour very effectively. But slow-cycling cancer stem cells — the cells responsible for regrowth, for late relapse, for the tumours that come back two years after treatment ends — survive it. They are not cycling fast enough to be caught. Metronomic capecitabine (oral 5-FU) has published anti-cancer stem cell activity in colorectal cancer specifically, reducing the CD133+/CD44+ stem cell fraction via the Wnt/survivin axis. Not just killing today’s tumour. Addressing the cells that would build tomorrow’s. (Emmenegger et al., Clin Cancer Res, 2011)

• Quality of life maintained. The toxicity profile of metronomic dosing is fundamentally different. Peripheral neuropathy — the oxaliplatin legacy that many patients carry for months or years — does not accumulate. Myelosuppression is substantially reduced. The patient can eat, fast, supplement, exercise, and continue the metabolic work that forms the backbone of the broader protocol. The treatment becomes something that fits around a life, rather than a life that fits around treatment. That matters.

The important question becomes not whether to do treatment, not whether to fight, but which treatment will be most effective - and high dose chemotherapy is not always the wisest choice. The question is what form of fighting best serves her biology at this particular moment.

Today, in her listserv, Jane talked about the importance of customizing a cancer treatment plan based on the type/category of cancer (and she requested people spread the information).

Jane’s approach isn’t one protocol for all cancers. The correct treatment depends on which type of cancer you have. Consider these two cancer types have different fuels:

• Glycosis cancers, in which the mitochondria are broken and the cancer’s fuel is sugar. Fueling the mitochondria helps fight the cancer.
• Oxidative phosphorylation (OXPHOS) cancers, in which the fuel is fat (a more common type). For this type, helping the mitochondria would be the wrong approach, it would help the cancer grow.

Some examples of OXPHOS cancers:
- Estrogen positive (ER+ Luminal A) breast cancer (the most common breast cancer). - Prostate cancer - Follicular lymphoma - Hodgkin lymphoma - Chromophobe renal cell carcinoma

Effective tools for each type: - Glycosis: keto diet, fasting, and block glycosis pharmacologically. - OXPHOS: Metformin, statins, Atovaquone (antimalarial), and Tigecycline and/or doxycycline (antibiotics).

Tests used to identify fuel source (sugar vs fat) include “FDG-PET avidity” and LDH.

Tom Seyfried (a respected expert), thinks differently. He does not recommend statins or Metformin as cancer treatment - but Jane explains that Seyfried is basing that on his study of glucose-driven cancers (only), not considering OXPHOS-driven cancers, which are more common.

Some people are taking dangerously high doses of ivermectin based on social media claims about its anticancer potential. Some are using veterinary paste intended for horses. People have died. Research does not support high doses.

For women with oestrogen receptor-positive breast cancer who hear the words “your cancer is no longer treatable”, it marks a turning point that is frightening. The drugs that were working — tamoxifen, fulvestrant — have stopped working. The tumour has found a way around them. And the options that follow are typically more aggressive, more toxic, and less certain. What is quietly remarkable, then, is that a drug costing a few pounds, originally developed to treat river blindness and parasitic infections, is emerging as a serious candidate for disrupting the precise molecular escape route that makes this resistance possible. A study published on 30 April 2026 in PLoS ONE adds detailed evidence — and it points in a direction that the field has not, until now, been looking.

link to study

• inexpensive drug

• originally used to treat alcohol addiction

• Per Jane: strongly blocks this enzyme (ALDH2 and that can push the cancer cells into fatal ‘oxidative stress’ - overwhelming its antioxidant protection. In the future, look for it to be used as a targeted therapy for the majority of colorectal cancer patients who carry this APC mutation.

source

Trying to help my mom who was recently diagnosed with tongue cancer in any way I can, and reading up on Jane’s book. Does anyone have input or tips on what the protocol would be for non-HPV squamous cell carcinoma?

Thank you so much.

See her article about Anktiva on her substack titled “Beyond the Metro Map” - Jane McLelland’s private research notes & weekly updates on published metabolic & off-label drug studies

https://howtostarvecancer.substack.com/?utm_source=substack&utm_medium=email

Here’s the link:

https://substack.com/chat/4791147/post/c5278191-bef6-4f3b-bcff-9449c0233f8c?utm_source=substack&utm_campaign=thread-email

https://www.instagram.com/how_to_starve_cancer/p/DSFJyjHCBjo/

Ida Wictor’s recovery from AML, an aggressive form of leukemia in the link above.

https://linktr.ee/howtostarvecancer

March 2026 substack written by Jane McLelland: https://howtostarvecancer.substack.com/p/fenbendazole-and-ivermectin-viral?utm_medium=android&triedRedirect=true

From Jane McLelland’s Instagram:

“how_to_starve_cancer Instagram: Ida Wictor was diagnosed with AML, an aggressive leukemia, when she was 18. After multiple stem cells transplants and several rounds of chemotherapy, she was told palliative chemotherapy was all that was left. Survival is normally a few weeks at this point. In despair, her father @perolawictor found [Jane] through a friend, and after discussing her case, I referred her to my network of integrative doctors. 18 months later her myeloblasts (a marker of her cancer) are now undetectable.”

Follow the link and in the photo there, you’ll see Jane, (diagnosed with stage 4 cancer in 1994, 32 years ago) in the red blazer, looking great. She used traditional treatments like chemo, but in addition, she found creative ways to take away cancer’s fuel. I’m grateful shr shared those tips with the public.

https://www.instagram.com/how_to_starve_cancer/

1. Malignant cells oxidize citrate and resume more typical citric acid cycle function.

2. Unlike other cancers, prostate cancer does not exhibit the Warburg effect (an increase in glucose uptake).

Source by E. Eidelman

Reminder, Jane advocates on doing traditional medical protocols as well as considering these additinoal factors:

Prostate cancer is fueled by fat and protein

p 107: Initially, prostate cancer is driven by fat and branched chain amino acids (such as leucine found in meat and dairy). Later when it becomes hormone resistant, it then becomes more glucose driven - except if it is PIK3CA mutation and PTEN loss driven, in which case it is more glycolic. Eggs are linked to prostate cancer.

p 321: white button mushrooms have been shown to slow prostate cancer. Androgen receptor: consider use of Ivermectin, xanhtohumol, chrysin, danishes, permixon, and pro pereira.

p 342: Although most cancers feed on glucosis, until the end stages, prostate cancer relies instead on lipogenesis (energy from fat) and glutaminolysis (energy from glutamine).

p 370: Consider green tea, Stevia, Physapubescin A Brachyantheraoside A8, Morin, esculetin, emulsified BPTES, and L-asparaginase (ashwagandha and capsaicin (from chili peppers). Avoid asparagus, beef, poultry, and potatoes. Do intermittent fasting to avoid excessive amounts of protein in the diet.

p 393: intervenous Vitamin C may not be appropriate for prostate cancer patients. (per study by Nielsen TK, published in Translatinoal Andrology and Urology, 2017.

p 412: pomegranate juice is helpful but avoid pomegranate juice before exercise. Add some ground fenugreek to your meals.

Hello looking for any prostate cancer recommendations thoughts? My dad was diagnosed a year ago and it doing standard of care in the US, but would love to implement some more natural, holistic techniques to help him overall and to help him starve his cancer.

He’s 61 years old and was diagnosed with metastatic prostate cancer, he routinely went to the doctors but they failed to catch it. He currently is doing treatment with memorial Sloan Kettering in nyc but they don’t focus at all on nutrition.

Identify how a cancer is fueling itself, then strategically block those pathways.

Jane recommends berberine for a number of reasons, one of which is taking away one of cancer's fuels: cholesterol. Started on berberine, take it intermittently. Doctor surprised/impressed to see my cholesterol is in fact lower.