Nicotine and Glioblastoma: Dr. Ardis on Brain Tumors

Table of Contents

1. 1. What Dr. Ardis Says
2. 2. A Plain Primer: What Glioblastoma Is
3. 3. Nicotinic Receptors on Glioblastoma Cells
4. 4. Looking for the 2021 Study
5. 5. Laboratory Studies of Nicotine and Tumour-Cell Growth
6. 6. Snake and Snail Toxins, and Receptor-Targeted Compounds
7. 7. Nicotine During Radiation and Temozolomide
8. 8. Smoking and Glioma in Large Population Studies
9. 9. Safety Notes
10. 10. Dr. Ardis’s Own Work
11. Key Research Papers
12. Connections
13. Featured Videos

1. What Dr. Ardis Says

Asked whether anything suggests that nicotine can shrink tumours or fight cancer, Dr. Ardis answers directly:

“Glioblastomas were proven in 2021 to be cured by nicotine alone in three days.”

He states that the finding is set out in his book, where he shows that researchers “were able to create a glioblastoma in 72 hours and then reverse it and shrink it by half in 72 hours with just nicotine.”

Asked whether any person with glioblastoma has seen this happen, he says yes: several medical doctors and oncologists, some in Spain and some in South America, are now using nicotine because of his presentations, in which he shows the research studies testing nicotine against glioblastomas and other cancers, and he reports that they are “finding remarkable results” and that tumours are shrinking. Later in the same conversation he says that people wondering about cancers and nicotine can speak with oncologists who are using it “to cure people of different cancers,” and names a physician in Spain who consults with patients. (This site does not name referral services or individual practitioners.)

On how much to use for something as serious as a brain tumour, Dr. Ardis does not give a tumour-specific dose. He says he always recommends starting slow, “because nicotine is going to be releasing poisons out of the body. It is a major detoxing nutrient.” He gives an example of starting too high: a 14 mg nicotine patch given to someone new to nicotine would bring “diarrhea galore,” and probably vomiting. For a person with a chronic illness who is starting nicotine, he recommends beginning with the smallest size, about 1 mg; he notes that nicotine gum is sold only in 2 mg and 4 mg pieces, so the 1 mg starting amount is not a gum. His full step-by-step approach is on the Nicotine Patch Protocol page.

The claim sits inside his wider argument, set out on the Nicotine Hypothesis page, that nicotine occupies the nicotinic acetylcholine receptors of the body and that many illnesses involve those receptors.

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2. A Plain Primer: What Glioblastoma Is

The brain is made of nerve cells (neurons) and a larger number of support cells called glial cells. Tumours that grow from glial cells are called gliomas. Doctors grade gliomas from 1 to 4 by how abnormal the cells look and how fast they grow. Glioblastoma (older name: glioblastoma multiforme, GBM) is the grade-4 form of astrocytoma, the glioma that grows from star-shaped astrocytes.

• How it behaves. Glioblastoma sends thin fingers of cells into the surrounding brain, which is why surgery cannot remove every cell and why it usually returns.
• Standard treatment. Surgery to remove as much as is safe, then radiation combined with temozolomide, an oral chemotherapy, followed by further cycles of temozolomide.
• Cell lines. Much of the research below uses glioblastoma cells grown in dishes. The most widely used line is U87 (also written U87MG); others include A172, T98G and “primary” cells taken directly from a patient’s tumour at surgery. A result in a dish tells researchers how cells respond to a chemical; it is the first step before animal and human studies.

The site’s full page on the disease, its symptoms and its treatment is Brain Cancer.

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3. Nicotinic Receptors on Glioblastoma Cells

Nicotine works by fitting into nicotinic acetylcholine receptors (nAChRs), small gated channels in the cell surface that normally open for the body’s own messenger, acetylcholine. They are built from five subunits, and the subunit mix gives each receptor type its name — α7, α9, α4β2 and so on. The site’s primer on them is Nicotinic Acetylcholine Receptors.

Several research groups have now shown that glioblastoma cells carry these receptors:

• A Milan team (Pucci and colleagues, 2021) found that U87MG cells and a temozolomide-resistant glioblastoma line called GBM5 carry the same set of nicotinic receptor types, with α7- and α9-containing receptors doing the signalling work.
• A German neurosurgery team (Kolodziej and colleagues, 2021) measured 28 genes of the acetylcholine system in 44 glioblastoma samples and 5 healthy brain samples. Most of the system was turned down in the tumours, with one exception: the gene for the α7 subunit, CHRNA7, stayed expressed in primary glioblastoma and in U87 cells.
• A Moscow team (Gondarenko and colleagues, 2024) demonstrated working α1-type, α7 and α9 receptors on several patient-derived glioblastoma cultures as well as on U87MG.
• A 2021 review of α9 receptors in cancer by the Milan group summarises that most cancer cells and tissues carry high levels of α9-containing receptors, and that these receptors take part in signals tied to cell growth, resistance to cell death and spread.

So the receptor that nicotine binds is present on glioblastoma cells. What the research reports about what happens when it is switched on, or blocked, is set out in the next three sections.

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4. Looking for the 2021 Study

Dr. Ardis names a 2021 study, a three-day (72-hour) time frame, and shrinkage by half. The specific study is not identified here with certainty, and the page does not have the passage of his book in which he presents it. Two papers that appeared in 2021 match parts of that description, and both are set out below as they read.

Kolodziej et al., 2021 — an α7 activator slows glioblastoma growth

Published in Oncology Letters in September 2021 by neurosurgeons at Justus-Liebig University Giessen, Germany. The team treated three glioblastoma cell lines (A172, U87 and G28) and primary cells from patients’ tumours with GTS-21, with acetylcholine, or with nicotine, at 6.25 to 50 micromolar, and measured how many cells were alive at 24, 48 and 72 hours.

• GTS-21 is a laboratory compound built from anabaseine, a natural nicotine-like substance found in certain marine worms; it switches on the α7 nicotinic receptor. It slowed glioblastoma cell growth in a dose- and time-dependent way.
• In eight primary tumour cultures treated for 48 hours, the median loss of growth was 51%, ranging from 36% to 84%.
• Blocking the α7 receptor with α-bungarotoxin, a snake venom toxin, restored growth in U87 cells but not in the other two lines.
• Nicotine and acetylcholine at the same concentrations had no effect on cell viability in this study.

The authors concluded that GTS-21 “may inhibit the proliferation of GBM cells and may therefore serve as a novel therapeutic approach,” which they say warrants further investigation.

Pucci et al., published online October 2021 — nicotinic-receptor compounds after 72 hours

Published in Pharmacological Research (online October 2021, issue January 2022). The Milan group tested two new compounds, StN-4 and StN-8, made by joining a molecule that acts on α7 and α9 nicotinic receptors (MG624) with a resveratrol-derived compound that targets the cell’s energy plants, the mitochondria. After 72 hours of exposure, both compounds reduced U87MG cell growth and cut the cells’ mitochondrial energy production; one of them (StN-4) also pushed cells into a resting phase and increased programmed cell death. They were less potent against normal mouse astrocytes than against the tumour cells.

Neither paper used a living animal or a patient, and neither grew a tumour and then shrank it; both measured cells in dishes. Readers who want to look further can use the PubMed searches listed under Key Research Papers.

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5. Laboratory Studies of Nicotine and Tumour-Cell Growth

Several laboratory studies have put nicotine itself, or nicotine-containing liquid, onto glioblastoma cells or into tumour-bearing mice. They are listed oldest first, with what each reports.

• Yamamura et al., 1998 (Showa University, Tokyo). Nicotine killed human glioma and glioblastoma cells (KG-1-C, GBS-1 and T98G) in a dose-dependent way. The cells did not show the DNA pattern typical of programmed cell death; nicotine caused a rapid rise of calcium inside the cells, most of all in the nucleus, which the authors propose is an early step in nicotine-induced cell death.
• Khalil et al., 2013 (University of Virginia). At concentrations comparable with those found in chronic smokers, nicotine increased migration, growth, colony formation and radiation resistance in U87 and GBM12 glioblastoma cells, acting through the EGFR growth-signal pathway and its downstream AKT and ERK signals. Blocking those pathways reduced the effects.
• Pucci et al., 2021 (Milan). Nicotine, and also choline (a nutrient that is raised in glioblastoma tissue), increased the growth rate of U87MG and temozolomide-resistant GBM5 cells and switched on the AKT and ERK pathways. Blocking α7 or α9 receptors, or silencing their genes, prevented the effect. The authors suggest these receptors “may contribute to the aggressive behaviour of this tumor” and may point to new treatment strategies.
• Kwon et al., 2021 (National Cancer Center, Korea). Electronic-cigarette liquid increased EGFR and ERK activation in brain-tumour cells in a dose-dependent way, and mice implanted with patient-derived brain-tumour cells and treated with the liquid had faster tumour growth on MRI than untreated mice.

A 2026 genetic study (Yu and colleagues, Zunyi, China) used Mendelian randomization — a method that uses inherited gene variants as a natural experiment — and reported a causal link between genetically predicted blood cotinine, the main breakdown product of nicotine, and glioblastoma, together with candidate target genes such as HIF1α and MMP2.

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6. Snake and Snail Toxins, and Receptor-Targeted Compounds

Because nicotinic receptors are the target of several snake and cone-snail toxins, researchers use those toxins as precise tools to switch particular receptor types off. This overlaps with the receptor argument Dr. Ardis makes on the Cobra Venom and Nicotine page.

• Gondarenko et al., 2024. On patient-derived glioblastoma cultures and U87MG cells, selective toxins that block α1-type, α7 and α9 receptors stimulated cell growth when nicotinic agonists were present.
• Kolodziej et al., 2021. α-Bungarotoxin, which blocks α7, restored growth of U87 cells that GTS-21 had slowed (section 4).
• Pucci et al., 2021. Peptide blockers selective for α7- and α9-containing receptors prevented nicotine and choline from speeding glioblastoma cell growth (section 5).
• The Milan stilbene compounds (2021–2022). Molecules designed to act on α7 and α9 receptors while also attacking tumour mitochondria reduced glioblastoma cell growth after 72 hours (section 4).

Read together, these laboratory papers show that the nicotinic receptors on glioblastoma cells respond to both switching on and switching off, and that the result depends on the cell line, the receptor type and the compound. The research groups describe the receptors as a possible target for future drugs.

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7. Nicotine During Radiation and Temozolomide

A 2019 review in Expert Review of Neurotherapeutics by McConnell, Carr and Litofsky (University of Missouri) gathered what is known about nicotine and glioblastoma treatment. It reports that roughly 16–28% of patients with glioblastoma continue to smoke after diagnosis and during treatment, notes that the published literature on how smoking and nicotine affect glioblastoma treatment and survival is sparse, and discusses the cell pathways in glioblastoma that nicotine might act on and how nicotine may contribute to resistance to chemotherapy. The authors write that understanding nicotine’s effect on treatment should let physicians give patients evidence-based guidance about nicotine products during treatment.

The Khalil 2013 study (section 5) is the laboratory work most often cited on this question: in its cell experiments, nicotine at smoker-level concentrations made glioblastoma cells more resistant to radiation. The Milan group’s 2021 paper used a temozolomide-resistant line (GBM5) and found that nicotine sped its growth through α7 and α9 receptors.

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8. Smoking and Glioma in Large Population Studies

Tobacco smoke carries nicotine together with thousands of other compounds, including N-nitroso compounds that cause brain tumours in animals, so researchers have asked for decades whether smokers develop glioma more often. The main pooled analyses report:

• Holick et al., 2007 (Harvard). Three large U.S. cohorts — the Health Professionals Follow-up Study and the Nurses’ Health Studies I and II — with 365 gliomas over more than five million person-years. No link was found between glioma and smoking status, amount, duration or age at starting, including after allowing for a delay between smoking and diagnosis.
• Mandelzweig et al., 2009 (Israel). A meta-analysis of 17 studies. Overall risk for ever-smokers was 1.06 (95% confidence interval 0.97–1.15), meaning no clear difference. Cohort studies alone showed a small rise (1.10), and past smokers in cohort studies 1.16; the authors concluded that overall smoking is not associated with glioma risk, while the small cohort signal remained to be clarified.
• Li et al., 2016. 24 studies and more than 2.3 million people: risk 1.04 for ever-smokers, 0.97 for current smokers and 1.07 for past smokers, none statistically significant. A small rise (1.13) appeared in women who had quit, and not in men.
• Shao et al., 2016. 25 studies: risk 0.98 for ever-smokers, with no dose-response relationship overall; people who started smoking at age 20 or older showed a modest rise (1.25).

A risk of 1.00 means the same rate as non-smokers; 1.10 would mean 10% more. Across these analyses the figures sit close to 1.00. These studies measure who develops a glioma, not how an existing tumour responds to nicotine; they do not separate nicotine from the rest of tobacco smoke, and none studied nicotine patches, gum or pouches.

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9. Safety Notes

• Children and pets. Nicotine is a poison at doses that are small for an adult and large for a child or animal. Used and unused patches, gum, pouches and e-liquid must be kept out of reach and disposed of folded sticky-side in; poison-control centres receive calls every year about children who chewed a patch or swallowed a pouch.
• Who should not use nicotine without their own physician’s supervision: pregnancy and breastfeeding; unstable heart disease, a recent heart attack, serious rhythm problems or uncontrolled high blood pressure; and people with a history of stroke. Nicotine also interacts with several medicines.
• People in cancer treatment. Anyone receiving radiation or chemotherapy for a brain tumour should tell the treating team about every product they take, nicotine included, since the laboratory studies above report effects of nicotine on glioblastoma cells and on radiation response.
• Starting doses. Dr. Ardis himself warns that too much too fast causes nausea, vomiting and diarrhoea, and recommends starting with the smallest size.

The full list of contraindications is on the Nicotine Patch Protocol page.

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10. Dr. Ardis’s Own Work

• Moving Beyond the COVID-19 Lies: Restoring Health and Hope for Humanity — the book in which he presents the glioblastoma research he describes.
• Dr. Bryan Ardis Hub — the wing’s main page: his nicotine hypothesis and snake-venom theory.
• Culture Apothecary, “Nicotine Is NOT the Villain” (2025) — the podcast appearance quoted in section 1.

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Key Research Papers

1. Kolodziej MA, Gött H, Kopischke B, Bender MKF, et al. (2021). Antiproliferative effect of GTS-21 in glioblastoma cells. Oncol Lett. — PubMed PMID: 34539863
2. Pucci S, Bolchi C, Bavo F, Pallavicini M, et al. (2022). Evidence of a dual mechanism of action underlying the anti-proliferative and cytotoxic effects of ammonium-alkyloxy-stilbene-based α7- and α9-nicotinic ligands on glioblastoma cells. Pharmacol Res. — PubMed PMID: 34756924
3. Pucci S, Fasoli F, Moretti M, Benfante R, et al. (2021). Choline and nicotine increase glioblastoma cell proliferation by binding and activating α7- and α9- containing nicotinic receptors. Pharmacol Res. — PubMed PMID: 33276105
4. Pucci S, Zoli M, Clementi F, Gotti C (2021). α9-Containing Nicotinic Receptors in Cancer. Front Cell Neurosci. — PubMed PMID: 35126059
5. Gondarenko E, Mazur D, Masliakova M, Ryabukha Y, et al. (2024). Subtype-Selective Peptide and Protein Neurotoxic Inhibitors of Nicotinic Acetylcholine Receptors Enhance Proliferation of Patient-Derived Glioblastoma Cell Lines. Toxins (Basel). — PubMed PMID: 38393158
6. Yamamura M, Amano Y, Sakagami H, Yamanaka Y, et al. (1998). Calcium mobilization during nicotine-induced cell death in human glioma and glioblastoma cell lines. Anticancer Res. — PubMed PMID: 9703899
7. Khalil AA, Jameson MJ, Broaddus WC, Lin PS, et al. (2013). Nicotine enhances proliferation, migration, and radioresistance of human malignant glioma cells through EGFR activation. Brain Tumor Pathol. — PubMed PMID: 22614999
8. Kwon HJ, Oh YT, Park S, Kim SS, et al. (2021). Analysis of electric cigarette liquid effect on mouse brain tumor growth through EGFR and ERK activation. PLoS One. — PubMed PMID: 34495991
9. McConnell DD, Carr SB, Litofsky NS (2019). Potential effects of nicotine on glioblastoma and chemoradiotherapy: a review. Expert Rev Neurother. — PubMed PMID: 31092064
10. Yu S, Long M, Huang N, Luo Y, et al. (2026). Investigating the potential risk of nicotine exposure on glioblastoma: Integrating Mendelian randomization and network toxicology analysis. Comput Biol Chem. — PubMed PMID: 41967427
11. Holick CN, Giovannucci EL, Rosner B, Stampfer MJ, et al. (2007). Prospective study of cigarette smoking and adult glioma: dosage, duration, and latency. Neuro Oncol. — PubMed PMID: 17504930
12. Mandelzweig L, Novikov I, Sadetzki S (2009). Smoking and risk of glioma: a meta-analysis. Cancer Causes Control. — PubMed PMID: 19568697
13. Li HX, Peng XX, Zong Q, Zhang K, et al. (2016). Cigarette smoking and risk of adult glioma: a meta-analysis of 24 observational studies involving more than 2.3 million individuals. Onco Targets Ther. — PubMed PMID: 27366088
14. Shao C, Zhao W, Qi Z, He J (2016). Smoking and Glioma Risk: Evidence From a Meta-Analysis of 25 Observational Studies. Medicine (Baltimore). — PubMed PMID: 26765433

PubMed Topic Searches

1. PubMed: Nicotine and glioblastoma
2. PubMed: α7 and α9 nicotinic receptors in glioblastoma
3. PubMed: Smoking and glioma risk

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Connections

• Dr. Bryan Ardis Hub — the wing’s main page: his nicotine hypothesis and snake-venom theory
• The Nicotine Hypothesis — his receptor argument in full
• Nicotinic Acetylcholine Receptors — the α7 and α9 receptors explained
• Nicotine Patch Protocol — his starting doses and the contraindications
• Cobra Venom and Nicotine — the receptor that venom toxins and nicotine share
• Detox and Recovery — his account of nicotine as a detoxing nutrient
• Moving Beyond the COVID-19 Lies — the book that presents the glioblastoma study he cites
• Brain Cancer — the site’s page on glioblastoma and other brain tumours
• Fenbendazole: Off-Label Cancer Use — another repurposed compound studied on glioblastoma cells
• Choline — the nutrient that also acts on α7 and α9 receptors

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