Lymphoma

Subtypes

Description

Cancer is uncontrolled cell growth driven by extreme metabolic dysfunction. Nearly all cancers are locked into the Warburg effect—they depend almost exclusively on glucose and glycolysis for energy. Large-scale metabolic profiling shows that ≈99.996% of all cancers are strictly carbohydrate-dependent. They cannot meaningfully use fat or ketones because they have:

No ketolytic enzyme expression
No transport capacity for ketones
No mitochondrial upregulation during ketosis
No survival advantage in a ketogenic metabolic state

Only a tiny minority (some melanoma and a few leukemias) show partial flexibility; the rest collapse without glucose. Most tumors massively overexpress IGF-1 receptors (often ~15× more than normal tissue), making them hypersensitive to insulin/IGF-1. This signaling reprograms metabolism so the tumor can steal and divert carbohydrates into nucleotides, lipids, and protein synthesis to fuel rapid growth. mTOR remains hyperactivated, autophagy is shut down, and chronic inflammation (IL-6, TNF-α) creates a pro-growth microenvironment.

Glucose dependence: Tumors upregulate GLUT transporters and glycolysis, making sugar their only viable fuel.
IGF-1 / insulin signalling: High receptor density drives continuous growth and blocks apoptosis.
mTOR overactivation: Constant "grow" signalling disables autophagy.
Inflammation: Cytokines promote mutation, angiogenesis, and tumor survival.

Because cancer cells are metabolically inflexible, ketosis hits them at every weak point. Fasting or ketogenic diet create a metabolic environment in which cancer cannot grow:

Glucose and insulin drop: cancer starves.
IGF-1 decreases: growth signalling shuts down.
mTOR is suppressed: the tumor loses its command to replicate.
Ketone levels rise: normal cells thrive, cancer cells cannot use them.
Autophagy activates: the body's natural chemotherapy that selectively destroys damaged or mutated cells while sparing healthy ones.

The combination of low glucose, low insulin/IGF-1, suppressed mTOR, reduced inflammation, and activated autophagy creates a metabolic state where most cancers cannot survive or proliferate.

Root Causes

Carbohydrate consumption

[ 1 ] Saeid Doaei et al. (2019) DOI PMID [ 2 ] Anna E Arthur et al. (2018) DOI PMID [ 3 ] Christian A Maino Vieytes et al. (2019) DOI PMID [ 4 ] Jian Huang et al. (2017) DOI PMID [ 5 ] Maria V Liberti et al. (2017) DOI PMID [ 6 ] Takahiko Nakagawa et al. (2020) DOI PMID [ 7 ] Siyuan Xia et al. (2017) DOI PMCID PMID

Insulin Resistance

[ 8 ] F S Facchini et al. (2001) DOI PMID

IGF-1 (Insulin-like Growth Factor 1)

[ 9 ] Pollak M et al. (2004) DOI PMID [ 10 ] Baserga R et al. (2003) DOI PMID [ 11 ] O Larsson et al. (2005) DOI PMID

Systemic Inflammation

[ 12 ] Balkwill F et al. (2001) DOI PMID

mTOR (Mechanistic Target of Rapamycin)

[ 13 ] Robert A. Saxton et al. (2017) DOI PMID [ 14 ] Alejo Efeyan et al. (2010) DOI PMID [ 15 ] David A Fruman et al. (2017) DOI PMID [ 16 ] Panomwat Amornphimoltham et al. (2008) DOI PMID [ 17 ] Ma'anit Shapira et al. (2006) DOI PMID [ 18 ] David T Teachey et al. (2006) DOI PMID

Treatment Options

Fasting

[ 19 ] Lee C et al. (2012) DOI PMID [ 20 ] Sagun Tiwari et al. (2022) DOI PMID [ 21 ] Sebastian Brandhorst et al. (2021) DOI PMID [ 22 ] Maira Di Tano et al. (2020) DOI PMID [ 23 ] Alessio Nencioni et al. (2019) DOI PMID [ 24 ] Yichun Xie et al. (2024) DOI PMID [ 25 ] Albin Sjölin et al. (2022) Link [ 26 ] Stefanie de Groot et al. (2019) DOI PMID [ 27 ] M Mansilla-Polo et al. (2024) DOI PMID [ 28 ] Ciara H O'Flanagan et al. (2017) DOI PMCID PMID

Ketogenic Diet

[ 29 ] Irene Caffa et al. (2020) DOI PMID [ 30 ] Salvatore Cortellino et al. (2023) DOI PMID [ 25 ] Albin Sjölin et al. (2022) Link [ 21 ] Sebastian Brandhorst et al. (2021) DOI PMID [ 31 ] Giulia Salvadori et al. (2021) DOI PMID [ 27 ] M Mansilla-Polo et al. (2024) DOI PMID

Susceptibilities

Autophagy

Sources

[1] Dietary Carbohydrate Promotes Cell Survival in Cancer Via the Up-Regulation of Fat Mass and Obesity-Associated Gene Expression Level

[ 1 ] Saeid Doaei et al. (2019) DOI PMID

[2] Higher carbohydrate intake is associated with increased risk of all-cause and disease-specific mortality in head and neck cancer patients: results from a prospective cohort study

[ 2 ] Anna E Arthur et al. (2018) DOI PMID

[3] Carbohydrate Nutrition and the Risk of Cancer

[ 3 ] Christian A Maino Vieytes et al. (2019) DOI PMID

[4] A meta-analysis between dietary carbohydrate intake and colorectal cancer risk: evidence from 17 observational studies

[ 4 ] Jian Huang et al. (2017) DOI PMID

[5] The Warburg Effect: How Does it Benefit Cancer Cells?

[ 5 ] Maria V Liberti et al. (2017) DOI PMID

[6] Fructose contributes to the Warburg effect for cancer growth

[ 6 ] Takahiko Nakagawa et al. (2020) DOI PMID

[7] Prevention of Dietary-Fat-Fueled Ketogenesis Attenuates BRAF V600E Tumor Growth

[ 7 ] Siyuan Xia et al. (2017) DOI PMCID PMID

[8] Insulin resistance as a predictor of age-related diseases

[ 8 ] F S Facchini et al. (2001) DOI PMID

[9] Insulin-like growth factor-I and risk of breast cancer by age and hormone receptor status

[ 9 ] Pollak M et al. (2004) DOI PMID

[10] The role of the IGF-I receptor in cancer

[ 10 ] Baserga R et al. (2003) DOI PMID

[11] Role of insulin-like growth factor 1 receptor signalling in cancer

[ 11 ] O Larsson et al. (2005) DOI PMID

[12] Inflammation and cancer: back to Virchow?

[ 12 ] Balkwill F et al. (2001) DOI PMID

[13] mTOR signaling in growth control and disease

[ 13 ] Robert A. Saxton et al. (2017) DOI PMID

[14] mTOR and cancer: many loops in one pathway

[ 14 ] Alejo Efeyan et al. (2010) DOI PMID

[15] The PI3K-AKT-mTOR pathway in human cancer: genetic alterations and therapeutic implications

[ 15 ] David A Fruman et al. (2017) DOI PMID

[16] Inhibition of mTOR by Rapamycin Causes the Regression of Carcinogen-Induced Skin Tumor Lesions

[ 16 ] Panomwat Amornphimoltham et al. (2008) DOI PMID

[17] The mTOR inhibitor rapamycin down-regulates the expression of the ubiquitin ligase subunit Skp2 in breast cancer cells

[ 17 ] Ma'anit Shapira et al. (2006) DOI PMID

[18] The mTOR inhibitor CCI-779 induces apoptosis and inhibits growth in preclinical models of primary adult human ALL

[ 18 ] David T Teachey et al. (2006) DOI PMID

[19] Fasting cycles retard growth of tumors and sensitize a range of cancer cell types to chemotherapy

[ 19 ] Lee C et al. (2012) DOI PMID

[20] Effect of fasting on cancer: A narrative review of scientific evidence

[ 20 ] Sagun Tiwari et al. (2022) DOI PMID

[21] Fasting and fasting-mimicking diets for chemotherapy augmentation

[ 21 ] Sebastian Brandhorst et al. (2021) DOI PMID

[22] Synergistic effect of fasting-mimicking diet and vitamin C against KRAS mutated cancers

[ 22 ] Maira Di Tano et al. (2020) DOI PMID

[23] Fasting and cancer: molecular mechanisms and clinical application

[ 23 ] Alessio Nencioni et al. (2019) DOI PMID

[24] Fasting as an Adjuvant Therapy for Cancer: Mechanism of Action and Clinical Practice

[ 24 ] Yichun Xie et al. (2024) DOI PMID

[25] Cancer whitepaper

[ 25 ] Albin Sjölin et al. (2022) Link

[26] Effects of short-term fasting on cancer treatment

[ 26 ] Stefanie de Groot et al. (2019) DOI PMID

[27] Popular Diets and Skin Effects: A Narrative Review

[ 27 ] M Mansilla-Polo et al. (2024) DOI PMID

[28] When less may be more: calorie restriction and response to cancer therapy

[ 28 ] Ciara H O'Flanagan et al. (2017) DOI PMCID PMID

[29] Fasting-mimicking diet and hormone therapy induce breast cancer regression

[ 29 ] Irene Caffa et al. (2020) DOI PMID

[30] Fasting mimicking diet in mice delays cancer growth and reduces immunotherapy-associated cardiovascular and systemic side effects

[ 30 ] Salvatore Cortellino et al. (2023) DOI PMID

[31] Intermittent and Periodic Fasting, Hormones, and Cancer Prevention

[ 31 ] Giulia Salvadori et al. (2021) DOI PMID