Why this matters

Jane McLelland was told her cancer was terminal. Stage IV, a tumour in the lung, no further options.

That was more than twenty years ago. She is still here, and she wrote a book about how she did it: How to Starve Cancer.

Professor Thomas Seyfried has spent four decades in the lab asking one question. What does a cancer cell actually eat?

I spent the last few weeks with both of them. Jane's book. Six of Seyfried's recent talks, transcribed. And a third book, The Cancer Resolution by Mark Lintern, that tries to connect them.

As a pharmacist, I wanted to know one thing: where do they agree, and what can you do with that today?

Because for many people with advanced cancer, the most frightening sentence is not the diagnosis.

It is "there is nothing more we can do."

What: cancer as a fuel problem

Healthy cells make most of their energy in the mitochondria, the small power plants inside each cell, using oxygen. That route — oxidative phosphorylation — gives roughly 30 to 36 units of energy (ATP) per molecule of glucose.

Cancer cells do something older and cruder. They ferment. Fermentation works without oxygen and gives about 2 ATP per glucose.

That is not a small difference.

Otto Warburg described this almost a hundred years ago — the Warburg effect. Seyfried took it further. In his view the mitochondria of cancer cells are damaged, so the cell falls back on fermentation — and it ferments two fuels:

• Glucose, turned into lactic acid in the cell.

• Glutamine, an amino acid, fermented inside the damaged mitochondria, with succinic acid as a by-product.

Take away both, and the cell runs out of energy. In his own words, from one of his recent talks:

Now, mind you — not everyone agrees on fat.

Jane McLelland's Metro Map includes fat as a third fuel line, and she describes some cancers, such as prostate cancer, as fat-hungry. Mark Lintern calls these extra fuels "a fly in the ointment".

Seyfried's answer is simple: in those experiments, the cells always still had glucose and glutamine available. Remove those two, he says, and fat cannot rescue them.

In a recent article, Jane puts it more sharply (McLelland, 2026). Tumours adapt. Some ramp up the machinery to take in fat and to use ketones. And no fuel line is ever fully closed — the body keeps making its own glucose, so the press is pressure, not a lock. In her words: "Cancer does not need every door open."

Her biggest concern is the person, not the tumour. Someone who is already losing weight — common in pancreatic cancer — can be harmed by strict restriction. Her answer is timing: short, well-placed ketogenic or fasting pulses alongside treatment, rather than permanent restriction.

Here is the part that matters for you. Whichever side is right about fat, all three agree on glucose and glutamine. That is where the plan starts.

What happens inside a fermenting cell

Why does it matter that a cell ferments? Because fermentation changes the whole chemistry of the cell — and of its neighbourhood.

It turns the surroundings acidic. Fermentation produces lactic acid, and glutamine fermentation adds succinic acid. The cell pumps the acid out, and the tissue around a tumour becomes markedly acidic. Seyfried describes a vicious circle: the acidity damages the mitochondria further, and each daughter cell inherits that damage. More damage, more fermentation, more acid.

It sends a false alarm. Succinic acid that builds up acts as a signal of oxygen shortage, even when oxygen is present. The cell answers by switching on even more of its fermentation machinery (Selak et al., 2005).

It upsets the cell's redox balance. Every process in a cell — reading DNA, building proteins, repairing damage — depends on a finely tuned balance of acidity and electrical charge (the redox balance, or ORP). When that balance shifts, these processes go off course. In Seyfried's view, this is also why cancer cells carry so many DNA mutations: they follow the mitochondrial damage, rather than cause it.

It switches off the self-destruct button. A damaged cell normally removes itself through programmed cell death — apoptosis. That switch sits in the mitochondria. When the mitochondria are damaged, the cell loses the ability to die when it should. It keeps dividing.

What damages the mitochondria in the first place?

Seyfried names many triggers: radiation, carcinogens, chronic inflammation, viruses, hypoxia, age. Mark Lintern goes a step further. He proposes that an infection — in his view a fungal one — drives the switch, as the cell's mitochondria use oxygen to fight the invader. Seyfried firmly rejects the idea that cancer is a parasite or an infection.

For what follows, the cause matters less than the result. Damaged or infected — in both views the cell ends up fermenting glucose and glutamine.

Sleep, stress and silent inflammation

Here I want to add a piece that rarely gets the attention it deserves.

Our body repairs itself on a schedule. The circadian rhythm — the internal day-night clock — coordinates when each organ system rests and restores. Deep sleep is when much of that repair happens.

Take that away — through stress, shift work, a work ethic that never switches off — and the repair falls behind. Low-grade, silent inflammation builds up. Inflammation damages mitochondria. And damaged mitochondria, as we have seen, fall back on fermentation.

This is not a fringe idea. The World Health Organization's cancer agency (IARC) classifies night shift work as "probably carcinogenic to humans", partly because of circadian disruption. And in Seyfried's talks, his clinical colleagues come back to sleep again and again.

That is not a small thing.

How: press and pulse

Seyfried calls his strategy press-pulse (Seyfried et al., 2017).

The press — every day

The press is steady, daily pressure on the cancer's fuel supply:

• A ketogenic metabolic therapy, low enough in carbohydrates that the body switches to burning fat and ketone bodies.

• Calorie restriction within that, as far as is safe for the person. Jane rightly warns that someone who is already losing weight needs to keep their strength first.

• Stress management and sound sleep — stress hormones raise blood sugar, and poor sleep feeds inflammation.

This is where the energy difference becomes your ally.

Your healthy cells, with working mitochondria, burn ketones and fatty acids fully. You keep your energy. According to Seyfried, the cancer cell cannot do this — it needs functioning mitochondria for these fuels, and those are exactly what it lacks.

So the same diet feeds you and puts the tumour under pressure.

Seyfried's group tracks this with the glucose-ketone index (GKI): blood glucose divided by blood ketones, measured with a simple meter at home (Meidenbauer et al., 2015). The lower the number, the deeper the metabolic pressure.

Seyfried's group has since put numbers on the press (Duraj et al., 2024): a GKI of 2 or lower, ideally 1, kept up continuously rather than in on-off cycles. Patients with enough body reserves may add a water-only or fasting-mimicking fast of 3 to 7 days every one to two months — planned and medically supervised, and not for anyone who is already losing weight.

The pulse — in waves

On top of the press come pulses: shorter, targeted hits against the fermentation pathways.

Seyfried mentions glutamine-targeting agents, compounds that slow glycolysis, and hyperbaric oxygen. The strongest glutamine blocker, DON, is not yet available for patients. His group recently showed in mice that the old anti-worm drug mebendazole targets both fuel pathways and works best when the animal is in ketosis (Mukherjee et al., 2026).

This is where Jane's Metro Map becomes a practical toolbox. She mapped off-patent drugs and supplements — metformin, berberine, statins, doxycycline and others — to the fuel lines they block. And she gives them in "kill phases", not all the time.

In her newer work she calls this a seven-lever stack (McLelland, 2026): diet, insulin control, fat metabolism, cancer stem cells, standard treatment, targeted pulses, and the gut microbiome and immune system. Her point: diet is one lever, not the whole protocol. And standard treatment stays in the stack.

The idea is the same in both: weaken the cancer with the press, then hit it while it is weak.

How long should a pulse last? Even Seyfried says: "we're working on that." Today it is the clinician's craft — start gently, watch the patient, and stop before the treatment does harm.

What if you want to use this?

What the evidence looks like today

Let me be straight with you, because you deserve that.

The strongest evidence so far comes from case reports and small studies. Seyfried describes Pablo Kelly, who lived almost eleven years with glioblastoma — "never cured", in Seyfried's words, but managed. The clinicians in these talks describe stage IV patients who "turned the ship around", and pancreatic cancer patients living three to five years, with a paper on the way.

Large randomised trials do not exist yet. Seyfried himself says the field is "not ready" for one — the details have to be worked out first, cancer by cancer. A framework for such a trial in glioblastoma has been published (Duraj et al., 2024).

Why so slow? Part of the answer is money. A diet and a handful of off-patent drugs have no sponsor. No company will fund a large trial for something it cannot patent.

So the data points are individual people. For someone who has been told "there is nothing more we can do," those people are not anecdotes. They are a direction.

What you can do

1. Measure. A blood glucose and ketone meter costs little. Learn your own GKI. Numbers make the press real.

2. Protect your sleep. Regular bedtimes, darkness, and a real end to the working day. Your mitochondria repair at night.

3. Find out your cancer's fuel. Jane and Lintern both stress this: tumours differ. Ask what is known about the metabolism of your specific cancer.

Jane has worked this out cancer by cancer (McLelland, 2026). She calls keto a precision tool, and sorts cancers by how they use fuel. Strict keto earns its place in glioma and glioblastoma — where, in her view, Seyfried's work is most clearly right — in BRAF-mutated melanoma, and as a four-to-eight-week start for people with clear insulin resistance. In pancreatic cancer she urges great caution: a 2026 randomised trial showed a survival signal (median 13.7 versus 10.2 months), but even under supervision patients stayed in ketosis on only 39% of days, and weight loss is the real danger. For hormone-driven and HER2-positive breast cancer, most colorectal cancer and advanced prostate cancer she prefers a low-glycaemic whole-food diet with a daily 16:8 eating window; in ER-positive ovarian and endometrial cancer she advises against keto altogether. And in AML, keto on its own is contraindicated: the leukaemic stem cells make their own ketones and use them as a shield. The best protocol, she adds, is the one you can keep up for years.

4. Bring it to your oncologist. Metabolic therapy works alongside treatment, and Jane herself combined it with low-dose chemotherapy. One question from these talks is worth taking along: "How will this treatment protect the health of my mitochondria?"

5. Look for a clinician trained in metabolic therapy. The press-pulse approach needs monitoring — especially calorie restriction and the pulses.

6. Read the sources below.

Simple but not simplistic.

Cancer is a fuel problem. And fuel is something you can influence — starting with your next meal, and tonight's sleep.

Let me know what you think.

Glossary

Apoptosis — Programmed cell death. The built-in self-destruct of a damaged cell. It is controlled by the mitochondria.

ATP (adenosine triphosphate) — The energy currency of the cell. Every process in the body is paid for in ATP.

Circadian rhythm — The body's internal 24-hour clock. It times sleep, hormone release and repair.

DON (6-diazo-5-oxo-L-norleucine) — A drug that blocks the use of glutamine. Effective in animal studies; not currently available for patients.

Fermentation — Making energy without oxygen. Fast but inefficient: about 2 ATP per glucose molecule.

Glucose-ketone index (GKI) — Blood glucose divided by blood ketones (both in mmol/L). A lower number means deeper ketosis and more pressure on the cancer's fuel supply.

Glutamine — The most abundant amino acid in the blood. The second fuel that cancer cells ferment, besides glucose.

Glycolysis — The first step in breaking down glucose, in the cell fluid outside the mitochondria. In cancer cells it ends in lactic acid.

Hyperbaric oxygen therapy (HBOT) — Breathing pure oxygen in a pressure chamber. Raises oxygen in the tissues; cancer cells cope badly with it.

Insulin resistance — The cells respond poorly to insulin, so the body makes more of it. Measured with fasting insulin or the HOMA-IR index.

Ketone bodies (ketones) — Fuels the liver makes from fat when carbohydrates are scarce. Healthy cells use them well; according to Seyfried, cancer cells cannot.

Ketosis — The metabolic state in which the body runs mainly on fat and ketones.

Lactic acid — The end product of glucose fermentation. Makes the tissue around a tumour acidic.

Mebendazole — An old, inexpensive anti-worm medicine, now studied for its effect on cancer metabolism.

Metabolic therapy — Treating cancer by targeting its energy supply, mainly through diet and drugs that block fuel pathways.

Metro Map — Jane McLelland's diagram of the fuel pathways of cancer, with the drugs and supplements that can block each one.

Mitochondria — The power plants of the cell. They burn fuel with oxygen and also control apoptosis.

Off-patent drug — An older medicine whose patent has expired. Cheap — and for that reason, rarely funded for new trials.

Oxidative phosphorylation (OXPHOS) — Energy production with oxygen in the mitochondria. Efficient: about 30–36 ATP per glucose molecule.

Oncologist — A doctor specialised in cancer treatment.

Press-pulse — Seyfried's strategy: constant pressure (the press) on the cancer's fuels, combined with short, targeted hits (the pulses).

Redox balance (ORP) — The balance between oxidising and reducing processes in the cell. It steers how DNA is read and how the cell repairs itself.

Succinic acid (succinate) — A by-product of glutamine fermentation. When it builds up, it signals a false oxygen shortage.

Warburg effect — Otto Warburg's observation that cancer cells ferment glucose even when oxygen is available.

Sources and further reading

Books

• McLelland, Jane. How to Starve Cancer… without starving yourself. ISBN 978-0-9519517-1-2. www.howtostarvecancer.com

• Seyfried, Thomas N. Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer. Wiley, 2012.

• Lintern, Mark. The Cancer Resolution? Cancer reinterpreted through another lens. 2023.

Scientific articles

• Warburg O. On the origin of cancer cells. Science 1956;123:309–314.

• Seyfried TN, Yu G, Maroon JC, D'Agostino DP. Press-pulse: a novel therapeutic strategy for the metabolic management of cancer. Nutrition & Metabolism 2017;14:19. https://pubmed.ncbi.nlm.nih.gov/28250801/

• Meidenbauer JJ, Mukherjee P, Seyfried TN. The glucose ketone index calculator: a simple tool to monitor therapeutic efficacy for metabolic management of brain cancer. Nutrition & Metabolism 2015;12:12. https://pmc.ncbi.nlm.nih.gov/articles/PMC4367849/

• Duraj T, et al. (Seyfried TN, senior author). Clinical research framework proposal for ketogenic metabolic therapy in glioblastoma. BMC Medicine 2024;22:578. https://doi.org/10.1186/s12916-024-03775-4

• HonorHealth Research Institute. Randomised phase II trial of a ketogenic diet in metastatic pancreatic cancer. Cancer 2026. PMID 41817106. https://pubmed.ncbi.nlm.nih.gov/41817106/

• Mukherjee P, et al. (Seyfried TN, senior author). Ketogenic diet as a metabolic vehicle enhancing the therapeutic efficacy of mebendazole and devimistat in juvenile syngeneic high-grade glioma. Cell Reports Medicine 2026. https://doi.org/10.1016/j.xcrm.2026.102845

• Selak MA, et al. Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-α prolyl hydroxylase. Cancer Cell 2005;7:77–85. https://pubmed.ncbi.nlm.nih.gov/15652751/

• Drenick EJ, et al. Resistance to symptomatic insulin reactions after fasting. Journal of Clinical Investigation 1972. https://pubmed.ncbi.nlm.nih.gov/5056667/

• IARC Monographs Volume 124: Night Shift Work. International Agency for Research on Cancer, 2020. https://www.iarc.who.int/news-events/iarc-monographs-volume-124-night-shift-work

• McLelland J. Closing the "Other Doors": Why Seyfried's Metabolic Model Is Harder to Translate Than It Sounds. Beyond the Metro Map (Substack), 18 August 2026. https://howtostarvecancer.substack.com/p/closing-the-other-doors-why-seyfrieds

• McLelland J. When Keto Works and When It Doesn't — A Cancer-by-Cancer Guide. Beyond the Metro Map (Substack), 13 July 2026 (paid article). https://howtostarvecancer.substack.com/p/when-keto-works-and-when-it-doesnt

• McLelland J. The Seven-Lever Metabolic Stack — What to Do When Keto Is Not the Answer. Beyond the Metro Map (Substack), 20 July 2026. https://howtostarvecancer.substack.com/p/the-seven-lever-metabolic-stack-what

Videos — Talking Cancer with Professor Thomas Seyfried (YouTube)

• Dr Thomas Seyfried's approach on metabolic therapy on cancer — https://www.youtube.com/watch?v=k1YdUSjBOPM

• The Two Fuels Cancer Needs to Survive — and How to Cut Them Off — https://www.youtube.com/watch?v=HZZxYRmU8-k

• These are two of the biggest cancer misconceptions  

• Emily Kaplan and Dr. Seyfried: The oncology field must understand these new cancer findings

• You Should Know This About Metabolic Cancer Therapy 

• Where Are The Clinicians That Facilitate Metabolic Cancer Therapy? (Parts 1–3)

Richard de Laat, Pharmacist (ret.) — The Healing Pharmacist™. This article is information, not medical advice. Please discuss any change in your treatment with your doctor.

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