Book Review: How to Starve Cancer, by Jane McLelland

How To Starve Cancer: A Critical Review of Jane McLelland's Metabolic Approach

Examining the Promise and Controversies of Multi-Target Cancer Treatment

Jane McLelland

Jane McLelland's journey from Stage 1b cervical cancer to lung metastasis led her to develop a multi-pathway approach combining conventional therapies with repurposed drugs, supplements, and lifestyle changes. While her metabolic "starvation" strategy offers intriguing insights into cancer treatment, significant questions remain about her claimed leukemia diagnosis and the actual role of her drug cocktail in her recovery.

Book Overview

Published: September 25, 2018
Pages: 404
ISBN: 9780951951736
Website: www.howtostarvecancer.com

Jane McLelland's book chronicles her 25-year battle with cancer, beginning with a Stage 1b cervical cancer diagnosis at age 30. What sets her story apart is her systematic approach to combining conventional treatments with repurposed drugs and targeted supplements, based on her understanding of cancer's metabolic vulnerabilities.

The Cancer Journey Timeline

1994: Diagnosed with Stage 1b cervical cancer at age 30. Underwent surgery, radiation therapy, and chemotherapy. Began dietary changes: eliminated sugar, wheat, and dairy; supplemented with vitamins C and E, plus glucosamine sulfate for knee pain.

1999: Cancer metastasized to lungs with a golf ball-sized tumor. Before surgery, she strategically took ginger, curcumin, and omega-3 to reduce inflammation. Her supplement regimen expanded to include green tea, ellagic acid, resveratrol, milk thistle, pycnogenol, B12, folate, glucosamine sulfate, and CLA.

2000: Underwent chemotherapy with Gemcitabine, Cisplatin, and 5-FU. Her SCC (squamous cell carcinoma) marker dropped dramatically from nearly 600 to 130 (normal range). Started intravenous vitamin C and began taking berberine before chemotherapy sessions.

2003: A controversial blood analysis revealed rouleaux formations, leading to concerns about blood abnormalities. Began her famous drug cocktail: metformin, statins, dipyridamole, aspirin, and etodolac. Continued intravenous vitamin C treatments.

2004: When SCC markers increased, she resumed her drug cocktail and restarted berberine. Within two months, markers normalized, and CT scans showed no disease progression.

The Leukemia Controversy

Critical Analysis: McLelland claims to have developed therapy-related leukemia but never presents an official oncologist diagnosis. Her conclusion is based solely on blood analysis from Dr. Kenyon, a practitioner barred from medicine in the UK. This ambiguity is crucial because she credits her drug cocktail with stopping "incurable" leukemia progression—a claim that requires rigorous medical verification.

The book's most controversial claim centers on McLelland's assertion that she developed and conquered therapy-related leukemia using her metabolic approach. When questioned directly in podcasts, she provides evasive answers about this diagnosis. This ambiguity raises important questions: Was her cancer potentially cured by conventional chemotherapy in 2000? The timeline certainly suggests this possibility.

The Metabolic "Metro Map"

McLelland's signature contribution is her metabolic pathway visualization—an isosceles triangle representing cancer stem cell nutrition:

• Triangle Base: Fatty acid pathway
• Left Side: Glutamine pathway
• Right Side: Glucose pathway
• Center: Acetyl-CoA (the metabolic hub)

This map guides readers toward specific drugs and supplements that theoretically block multiple cancer fuel sources simultaneously—the essence of her "starvation" strategy.

The Intravenous Vitamin C Misattribution

McLelland incorrectly claims that Linus Pauling advocated intravenous vitamin C administration. Historical evidence shows Pauling consistently favored oral vitamin C, taking 12-18 grams daily in crystal form. This misattribution undermines the credibility of her vitamin C recommendations.

Repurposed Drug Insights

The book's most valuable contribution may be its comprehensive coverage of repurposed drugs for cancer treatment. McLelland was pioneering in using medications like metformin, statins, and dipyridamole for cancer—approaches that have since gained scientific interest and clinical investigation.

Her drug combinations target multiple pathways:

• Metformin: Metabolic disruption, mTOR pathway inhibition
• Statins: Cholesterol synthesis blockade
• Dipyridamole: Adenosine pathway interference
• Aspirin: Anti-inflammatory and anti-platelet effects
• Berberine: AMPK activation, glucose metabolism disruption

Critical Assessment

Strengths: Pioneering work in metabolic cancer treatment, comprehensive drug repurposing information, systematic multi-pathway approach, early adoption of now-validated concepts like cancer metabolism targeting.

Weaknesses: Unverified leukemia diagnosis, historical inaccuracies about vitamin C research, overly dramatic portrayal of medical system, harsh judgment of oncologists whose treatments likely contributed significantly to her recovery.

Bottom Line

McLelland's book offers valuable insights into metabolic approaches to cancer treatment and drug repurposing strategies. However, readers should approach her claims critically, particularly regarding her leukemia diagnosis and the relative contributions of conventional versus alternative treatments to her survival.

The book's true value lies not in its personal narrative but in its systematic approach to multi-pathway cancer treatment—an concept increasingly supported by current cancer research. For patients with advanced cancer, this book should be read alongside professional medical guidance, not as a substitute for evidence-based care.

⚠️ If you're exploring IV Vitamin C therapy, this article details critical factors to consider.

Last updated: March 24, 2025

ATF4 and FAM129A protein expression is increased in PCa

In this study, in vivo therapeutic silencing of the ATF4-FAM129A axis markedly inhibited tumor growth in a preclinical PCa model.

Ursolic acid and Tomatidine, as potential agents and/or lead compounds for reducing ATF4 activity.

References

Pällmann, N., Livgård, M., Tesikova, M. et al. Regulation of the unfolded protein response through ATF4 and FAM129A in prostate cancer. Oncogene 38, 6301–6318 (2019). https://doi.org/10.1038/s41388-019-0879-2

Ebert SM, Dyle MC, Bullard SA, Dierdorff JM, Murry DJ, Fox DK, Bongers KS, Lira VA, Meyerholz DK, Talley JJ, Adams CM. Identification and Small Molecule Inhibition of an Activating Transcription Factor 4 (ATF4)-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy. J Biol Chem. 2015 Oct 16;290(42):25497-511. doi: 10.1074/jbc.M115.681445. Epub 2015 Sep 3. PMID: 26338703; PMCID: PMC4646196.

Ovarian Cancer Treatment

Ovarian Cancer Treatments: Comprehensive Study Overview

Evidence-Based Analysis of Conventional, Repurposed, and Natural Therapies

Ovarian cancer is fundamentally a VEGF (vascular endothelial growth factor) driven tumor, making angiogenesis inhibition a critical therapeutic strategy. This comprehensive overview analyzes treatment options based on clinical evidence, focusing on overall survival (OS) improvements. Studies with significant OS benefits (>2x survival or HR < 0.75) are highlighted with 🔥 markers. The analysis covers conventional therapies, repurposed medications, and natural compounds with demonstrated anticancer activity.

⚠️ Important Medical Disclaimer: This information is for educational purposes only and should not replace professional medical advice. Always consult healthcare professionals before making treatment decisions. The studies presented here represent research findings that may not apply to all patients or clinical situations.

Top Overall Survival (OS) Benefits

🔥 Treatment	OS Benefit	Population	Study
Itraconazole + Chemotherapy	642 vs. 139 days (~4.6x)	55 patients, mixed stages	PMID: 24778064
Cimetidine	20% to 60% late-stage survival (3x)	Late-stage ovarian cancer	**Clinical reports**
Olaparib (SOLO1)	Not reached vs. 75.2 months (HR 0.55)	BRCA-mutated, first-line maintenance	JCO 2021
IV Vitamin C + Chemotherapy	58.6 vs. 42.8 months (HR 0.61)	Advanced ovarian cancer	Ma et al. 2014
Weekly Paclitaxel + Carboplatin	47.7 vs. 39.3 months (HR 0.69)	High-risk stage III/IV	ICON8
Green Tea Consumption	77.9% vs. 47.9% survival (~1.6x)	244 patients, observational	PMID: 15382073
Delta-Tocotrienol + Bevacizumab	Doubled survival rate, 70% disease stabilization in resistant cases	Enhanced anti-angiogenic activity	PMID: 30639384

Overall Survival Comparison

1. Conventional Chemotherapy Agents

Standard chemotherapy forms the backbone of ovarian cancer treatment, with platinum-based combinations showing the greatest efficacy. This section covers FDA-approved agents and their documented synergies with natural compounds.

Drug/Combination	FDA Approval	Key Outcomes	Notable Synergies
Cisplatin	1978	Foundation of platinum-based therapy	Curcumin, Melatonin, Berberine, Resveratrol, Ursolic Acid, Ashwagandha
Carboplatin + Paclitaxel	1991/1992	Standard first-line combination	Vitamin D3, I3C + EGCG, Modified Citrus Pectin
🔥 Weekly Paclitaxel + Carboplatin	Modified regimen	47.7 vs 39.3 months OS (HR 0.69) in high-risk patients	Enhanced with natural compounds
Topotecan	1996	Second-line therapy	Low-dose + Bevacizumab shows promise
Pegylated Liposomal Doxorubicin	2000	Reduced cardiac toxicity vs standard doxorubicin	Curcumin, Melatonin
Gemcitabine + Carboplatin	2006	Effective in stage IV disease	Reduced-dose schedule shows promise

2. Angiogenesis Inhibition: Targeting the VEGF-Driven Nature

Ovarian cancer is fundamentally a VEGF (vascular endothelial growth factor) driven tumor, making angiogenesis inhibition a cornerstone therapeutic approach. Targeting the tumor's blood supply offers multiple advantages including reduced metastatic potential and enhanced chemotherapy delivery.

Agent	Type	Mechanism	Clinical Evidence
Bevacizumab (Avastin)	Monoclonal Antibody	Direct VEGF binding and neutralization	Phase III trials show PFS benefit; OS results mixed
🔥 Delta-Tocotrienol + Bevacizumab	Natural + Targeted	Enhanced anti-angiogenic activity	Doubled survival rate, 70% disease stabilization in resistant cases
Theobromine	Natural Methylxanthine	VEGF pathway inhibition, PGP modulation	Preclinical studies demonstrate potent anti-angiogenic effects
🔥 Green Tea (EGCG)	Natural Polyphenol	Multi-target angiogenesis inhibition	77.9% vs 47.9% survival in regular consumers
Curcumin	Natural Polyphenol	VEGF downregulation, HIF-1α inhibition	Synergistic with chemotherapy, multiple trials
Ashwagandha	Adaptogenic Herb	VEGF receptor modulation	Synergy with cisplatin demonstrated
Ginger	Natural Gingerols	VEGF expression suppression	Anti-angiogenic effects in cancer models
Grape Seed Extract	Natural Proanthocyanidins	Endothelial cell proliferation inhibition	Preclinical anti-angiogenic activity

VEGF-Targeting Strategy:

Primary Approach: Bevacizumab remains the gold standard for VEGF inhibition in ovarian cancer
Enhanced Efficacy: Natural compounds like delta-tocotrienol can significantly enhance anti-angiogenic effects
Dietary Approach: Regular consumption of anti-angiogenic foods (green tea, dark chocolate, ginger) may provide complementary benefits
Combination Potential: Natural angiogenesis inhibitors show synergy with both conventional chemotherapy and targeted agents

3. Targeted Therapies

Targeted therapies represent precision medicine approaches, focusing on specific molecular pathways dysregulated in ovarian cancer.

PARP Inhibitors

Agent	Approval	Key Study	OS Outcome
🔥 Olaparib BRCA-mutated	2018	SOLO1 (7-year follow-up)	Not reached vs 75.2 months (HR 0.55); 67% vs 46% alive at 7 years
Olaparib + Bevacizumab	Combination	PAOLA-1	73.2 vs 65.5 months (HR 0.78) in HRD-positive
Niraparib	2017	NOVA	No OS difference in platinum-sensitive recurrent
Rucaparib	2016	ARIEL3	Maintenance therapy, OS data pending

Antibody-Drug Conjugates

Agent	Target	Study	OS Benefit
🔥 Mirvetuximab Soravtansine	Folate Receptor-α	MIRASOL	16.5 vs 12.7 months (HR 0.67) in platinum-resistant, FR-α high

4. Repurposed Drugs

Repurposed medications offer cost-effective treatment options with established safety profiles and demonstrated anticancer activity in ovarian cancer models.

Drug	Original Use	Mechanism in Cancer	Clinical Evidence
🔥 Itraconazole	Antifungal	Hedgehog pathway inhibition, angiogenesis suppression	OS 642 vs 139 days when combined with chemotherapy (n=55)
🔥 Cimetidine	H2 receptor antagonist	Immune modulation, angiogenesis inhibition	Late-stage survival improved from 20% to 60%
Metformin	Diabetes medication	mTOR inhibition, AMPK activation	Synergy with bevacizumab, reduces NGF effects
Clarithromycin	Antibiotic	Autophagy modulation, apoptosis induction	Synergistic with cisplatin in vitro and in vivo
Mebendazole	Antiparasitic	Tubulin disruption, VEGF inhibition	Combination with PRIMA1MET shows promise

5. Natural Compounds with Anticancer Activity

Natural compounds offer complementary therapeutic approaches with multiple mechanisms of action and favorable safety profiles.

High-Impact Natural Agents

Compound	Source	Mechanism	Clinical Evidence
🔥 High-Dose IV Vitamin C	Ascorbic Acid	Pro-oxidant effects at high doses	OS 58.6 vs 42.8 months (HR 0.61) with chemotherapy
🔥 Aspirin (Low-dose)	Salicylic Acid	COX inhibition, anti-inflammatory	20-34% risk reduction for ovarian cancer
Curcumin	Turmeric	NF-κB inhibition, VEGF suppression	Synergy with cisplatin, PLD, chemotherapy agents
I3C + EGCG	Cruciferous + Green Tea	Synergistic anticancer effects	Enhanced paclitaxel efficacy, long-term maintenance benefits
Vitamin D/Calcitriol	Cholecalciferol	VDR pathway activation	Enhances survival, useful addition to treatment
Modified Citrus Pectin	Citrus peels	Galectin-3 binding, metastasis inhibition	Synergy with paclitaxel, multiple studies

Natural PARP Inhibitors

Compound	Primary Source	PARP Inhibition	Additional Benefits
Quercetin	Capers, Red Onions, Dark Chocolate	Direct PARP-1 inhibition	Anti-inflammatory, antioxidant
Chlorogenic Acid	Green Coffee Bean	PARP-1 modulation	Metabolic benefits
Niacinamide	Vitamin B3	Competitive PARP inhibition	NAD+ pathway modulation
Puerarin	Kudzu Root	PARP-1 activity reduction	Cardiovascular protection

⚠️ Important Medical Disclaimer: This content is for educational and informational purposes only and should never replace professional medical advice, diagnosis, or treatment. The information presented is based on published research but may not reflect the most current clinical guidelines or individual patient circumstances. Treatment decisions should always be made in consultation with qualified healthcare professionals who can assess individual patient factors, contraindications, and current treatment protocols.

Research Status: Many natural compounds and repurposed drugs mentioned are in preclinical or early clinical development. Their safety and efficacy profiles may not be fully established for ovarian cancer treatment. Always discuss any complementary approaches with your oncology team.

Last updated: September 14, 2025