Lifestyle Oncology Learning Academy

Where treatment ends, lifestyle is the new beginning.  Lifestyle Oncology Learning Academy (LOLA) is my multi-faceted sandbox for learning and maintaining an anti-cancer lifestyle through management of the 3M’s: Metabolism, Malnutrition and Mayhem.

What is Cancer Metabolism?

Cancer metabolism refers to the alterations in cellular metabolism pathways that are evident in cancer cells compared with most normal tissue cells”.

I’m beginning to understand cancer metabolism within the context of the micro-environment and I found the topic very interesting since I read ‘How to Starve Cancer‘ (HTSC) by Jane McLelland who survived stage IV terminal cancer 19 years ago through her “spot of bother” action plan. Thank you to Jane for introducing me to this topic. I think the neat thing about this theory, from my perspective, is that I can see a way to possibly mitigate my risks in a way that is more within my control than just accepting watchful waiting. This theory is evolved from the Warburg Effect1; which has more recently been revisited by Thomas N. Seyfried, Travis Christofferson and Dr. Nasha Winters & Jess Higgins Kelley. Are all of these eminent scientists barking up the wrong tree? It seems unlikely. The current challenge is the tailoring for each cancer metabolic phenotype.

Mapping my Metabolic Phenotype (ER+/PR+ 8/8 HER2-)
Since Jane McLelland invented a ‘Metro Map’ diagram (featured here) to help people model their own cancer type, this complex topic is more communicable to non-specialists.  I’ve put the ‘Metro Map’ to the test against my ER+ metabolic phenotype which I found here (an excellent publication, thank you to the authors; citation in footnote2).  I appreciate the phenotype mapping is still an emerging science but I’m happy to look at the research scientists have achieved so far and “have a go”.  There are also many other signalling pathways and growth factors mentioned in the ‘HTSC’ book but I’m just looking at metabolism based on the ‘Metro Map’ for the purpose of this experiment.  

With permission from Jane McLelland in advance, I have applied the McLelland ‘Metro Map’ to my metabolic phenotype (ER+).  The suggested off-label drugs like metformin and statins or supplements like berberine, for example, to block these fuel lines [pathways] can be found in the ‘HTSC’ book against the McLelland ‘Metro Map’ on page 319.  The Care Oncology Clinic offer a protocol prescribing some of the drugs mentioned: more information can be found here.  Here is research on Neoadjuvant Metforminand breast cancer.  The following research paper explores a link between diabetes and cancer and the use of metformin for DNA repair.

So, here is my ER+ metabolic phenotype: no guarantee of it’s correctness is given or implied based on this being an emerging science but this feels like excellent progress. 

1. Glucose Pathways
– Glycolysis + MCT1 
– Glut 1 (Glucose Transporter 1)
– Lactate I’ve added this to the list as it is a key driver for glucose utilisation.  I target lactate with Magnesium supplements.   Magnesium is essential for the metabolism of Vitamin D so those Vitamin Dsupplements may do nothing if there is a deficiency in magnesium.  Vitamin D assists the homeostasis of Calcium and Vitamin K2 helps to transport Calcium to the bone and away from soft tissue.  (I have a history of fibroadenoma so for me this feels pretty important.)  I don’t take calcium supplements as I don’t want excess calcium levels, just healthy levels from plant-based foods. This publication discusses excess calcium levels (hypercalcemia) and breast cancer. If calcium levels drop too low the bone tissue will release calcium back into the system.  This publication confirms Metformin may be a therapeutic target for lactate which I have recently starting taking on the COC protocol.  The following research paper suggests lactate may be involved in progression and resistancy to therapy.  This research paper further confirms new roles discovered in lactate in the tumour micro environment.

PP Pathway (Pentose Phosphate Pathway) although this pathway is mentioned in the model I’ve referred to, it does not appear to be highly expressed in ER+ (Luminal A) tumours according to this publication3  so until I read anything to the contrary, I will not include this pathway for my phenotype.  The Pentose pathway runs in parallel with glycolysis which I’ve already targeted.  I’m of the opinion that targeting the PP Pathway with ER+ breast cancer is dangerous.  DHEA is the popular target for the PP Pathway which interferes with Tamoxifen and aromatase inhibitors and may increase progression.

2. Fatty Acid Pathways
– FASN/FAS (Acetyl CoA) 
– ACLY  (ATP Citrate Lyase/TCA Cycle)

3. Glutamine Pathways
– GS (Glutaminolysis)
– IGF-14 (not in the ER+ phenotype diagram I’ve used, but I feel it is essential that IGF-1 be targeted for ER+. I’ve read extensively on IGF-1 and I avoid consumption of all foods which may fuel this pathway (all animal products, including dairy).

So that’s a neat little experiment and the book How to Starve Cancer explains everything in context.  It’s a lot of knowledge for a reasonable price and it’s the best cancer book I’ve come across and I’ve read quite a few.  You can join the “Jane McLelland Off Label Drugs for Cancer” facebook group here which is a safe space for discussion.

In addition, the generic pathways which Jane suggests targeting, as a minimum, are listed on p328 of ‘How to Starve Cancer’.  The list includes IGF-1 for all cancers so it is reasonable that I have added it to the list for ER+ breast cancer anyway.  In ‘How to Starve Cancer’ there is information on abnormal cell signalling and growth factors and treatment suggestions for blocking them, with full citation/referencing.  I have focused on the metabolism ‘Metro Map’ as I was stage 3 at diagnosis and will primarily use metabolism for  recurrence prevention with a short-term blast at IBC for good measure, shown below.    For stage IV cancer there are additional suggestions designed to work alongside conventional treatment.  Jane is not suggesting a replacement for conventional medicine…..  ‘Integrated Oncology’ is the aim which I am fully in favour of.

From everything I’ve read so far on cancer metabolism, blocking pathways 1 (glucose) and 2 (fatty acid) above may up-regulate 3 (glutamine) so it’s important to block all three. The more advanced the cancer, the more it switches to more aggressive 3 (glutamine) and beyond this it moves to MMPs and Macropinocytosis (this is explained nicely on page 326 & 327).

Inflammatory Breast Cancer (IBC) has a relatively unknown micro-environment.  This means there is no metabolic phenotype specific to IBC as yet. 

In addition to my ER+ metabolic phenotype, I’m going to run with the following research papers in the meantime under three assumptions which turned out to be four assumptions after I discovered there is another metastatic route in aggressive cancers. This disease has more facets than a diamond! Assumptions:
1. IBC has metastatic(5a) tendencies, transitioning from epithelial to mesenchymal (EMT) so I’ve added to the discussion: epithelial E-Cadherin and mesenchymal Fibronectin suppression(5c).
2. IBC has an increased risk of higher levels of EGFR(6b) (full paper here)
3. EMT is not the only metastatic route in aggressive cancers according to this research paper(5b) Another pathway to add to the list for Non-EMT is the p53/p21 pathway.
4. The inflammatory nature may be an auto-immune feature similar to multiple myloma(6a) and rheumatoid arthritis (I have a long history of respiratory allergies (rhinitis/asthma) so I feel inclined to include autophagy(6a2) in the hypothesis for me)

With these assumptions in mind I will be adding the following pathway targets for IBC.  This may be overkill but I’d rather over-prevent than under-prevent.  The list looks more daunting than it is as some of the drugs target multiple pathways and the treatments for my ER+ metabolic phenotype has already covered some of these pathways.  I’ve added page references to the book where I’ve found the relevant pathway/marker in the book, otherwise I’ve referenced a research paper. 

EGFR (page 312/378)
COX2 (page 358)
TAMs/Macrophages (M2) (page 349/350) The significance of macrophages and immunity is discussed in the following research paper6c for all breast cancer types.
MMP-2 (page 346)
MMP-3 (page 346)
MMP-9 (page 346)
Autophagy/Macropinocytosis (page 337)
TGFB (page 345) IBC specific research
Snail1, E-Cadherin promotes CTC clustering (Panax Ginseng)
VEGF (page 345/381)
Ras/Kras (page 378)
OXPHOS (page 319 ‘Metro Map’)
Th2/IL response (page 381)

Stat3, Notch, NF-κB, Wnt/B-catenin, mTOR (page 308-310 & 369)
This research paper suggests Notch signalling is important in metastases(6d1) early on before progression, developing from the bone marrow/osteoblasts. Further confirmation of this along with associated signalling and markers NF-κB and IL6 in this research paper(6d2)

NF-κB hyperactivation is a common feature in IBC according to this research paper(6d3) and this research paper(6e) suggests metformin inhibits NF-κB activity; a pathway involved in regulating M1/M2 (macrophage) expression. This research paper(6f) also suggest CBD may be a promising therapy for NF-κB signalling events as well as inhibiting proinflammatory cytokines.

The STAT3 pathway has been researched(6f2) in relation to endocrine drug resistance. This study involved a drug developed from a stabilised form of Sulphoraphane (a component of cruciferous vegetables). Further confirmation of IL6/STAT3 involvement in metasteses is demonstrated in this research paper(6f3) which shows the drug ruxolitinib decreases breast cancer invasion in vivo demonstrating the potential for IL6/STAT3 targeted therapies for ER+ breast cancer

p53/p216g & glycolysis (page 378)

CDK4/6: recent studies(6h) have shown positive results for inhibitors of this pathway for metastatic hormone positive bc but in the long term there is a need to overcome drug resistance. The following research paper(6i) suggests blue green algae (spirulina platensis) combined with selenium may inhibit the growth of MCF7 and subsequently CDK4 and CDK6 as well as increasing the level of tumour supressor p53/p21. Further research on microalgae as an anti-cancer agent against multiple targets here(6j)

A recent study suggests decreased levels of GLA and EPA fatty acids(6k) were found in Inflammatory Breast Cancer breast adipose (fat) tissue. To balance any potential deficiency, I take a GLA (Gamma Linolenic Acid) supplement which can be found in evening primrose oil, blackcurrant seed oil, starflower/borage seed oil, hemp seed oil, and also in edible hemp seeds, oats, barley and spirulina. I also take an EPA (Eicosapentaenoic Acid) supplement which can be found in algae oil, seaweed, nuts, sunflower seeds. More info here

The following website has more information on inhibitors (blockers) against different targets.

This research paper is excellent for describing the complexity of EMT factors and Metabolism in cancers in general

If you are a researcher you may also be interested in this project:


Within the field of metabolism, exercise is very important for reducing breast cancer recurrence risk. Current thinking suggests it increases blood oxygen levels, burns excess calories (building muscle also increases metabolism) and reduces body fat. Here is an extract from a relevant publication(7) which suggests:

“…at least 30 minutes of moderate-intensity physical activity at least five days of the week, or 75 minutes of more vigorous exercise, along with two to three weekly strength training sessions, including exercises for major muscle groups. This recommendation has been endorsed by both the Canadian Cancer Society and the American Cancer Society.”

It does feel like a big effort at first but gradually becomes part of everyday life and you don’t have to think about it once it’s committed to autopilot. 


Nightly fasting(8) for more than 13 hours has been associated with reduced risk of breast cancer recurrence in vivo.


I keep my BMI below 24 as there is increasing evidence that maintaining a BMI below 24 improves recurrence risks. Obesity(9) is associated with poorer outcomes10. The body (adipose) fat stores oestrogen so increased weight means greater oestrogen stores; especially important in ER+ breast cancer. Before my diagnosis I was about a stone heavier, my BMI is now around 21.


1 The Warburg effect:  How does it benefit Cancer Cells?

The Warburg Effect and the Hallmarks of Cancer

2 Elia, Ilaria & Schmieder, Roberta & Christen, Stefan & Fendt, Sarah-Maria. (2016). Organ-Specific Cancer Metabolism and Its Potential for Therapy. Handbook of experimental pharmacology. 233. 321-353. 10.1007/164_2015_10. 

3 Expression of Pentose Phosphate Pathway-Related Proteins in Breast Cancer

Insulin-like growth factor 1 (IGF1), IGF binding protein 3 (IGFBP3), and breast cancer risk: pooled individual data analysis of 17 prospective studies.

5a Epithelial-Mesenchymal Transition Phenotype Is Associated with Clinicopathological Factors That Indicate Aggressive Biological Behavior and Poor Clinical Outcomes in Invasive Breast Cancer

5b Aggressiveness of non-EMT breast cancer cells relies on FBXO11 activity

5c Berberine Suppresses Fibronectin Expression through Inhibition of c-Jun Phosphorylation in Breast Cancer Cells

6a Autophagy inhibition enhances isobavachalcone-induced cell death in multiple myeloma cells.

6a2 The Therapeutic and Pathogenic Role of Autophagy in Autoimmune Diseases

6b EGFR signaling promotes inflammation and cancer stem-like activity in inflammatory breast cancer

6c A Single-Cell Atlas of the Tumor and Immune Ecosystem of Human Breast Cancer

6d1 Notch2 pathway mediates breast cancer cellular dormancy and mobilisation in bone and contributes to haematopoietic stem cell mimicry

Notch3 inhibits cell proliferation and tumorigenesis and predicts better prognosis in breast cancer through transactivating PTEN

6d2  Microenvironmental IL1β promotes breast cancer metastatic colonisation in the bone via activation of Wnt signalling

6d3 Distinct molecular phenotype of inflammatory breast cancer compared to non-inflammatory breast cancer using Affymetrix-based genome-wide gene-expression analysis

6e Metformin-treated cancer cells modulate macrophage polarization through AMPK-NF-κB signaling

6f  Cannabidiol prevents LPS‐induced microglial inflammation by inhibiting ROS/NF‐κB‐dependent signaling and glucose consumption

6f2 Targeting STAT3 signalling using stabilised sulphoraphane (SFX-01) inhibits endocrine resistant stem-like cells in ER positive breast cancer

6f3 IL6/STAT3 Signalling Hijaks Estrogen Receptor a Enhancers to Drive Breast Cancer Metastasis

6g Emerging Roles of p53 Family Members in Glucose Metabolism

6h  CDK 4/6 Inhibitors in Breast Cancer: Current Controversies and Future Directions

6i  Simultaneous Inhibition of Cell-Cycle, Proliferation, Survival, Metastatic Pathways and Induction of Apoptosis in Breast Cancer Cells by a Phytochemical Super-Cocktail: Genes That Underpin Its Mode of Action

6j  Microalgae in modern cancer therapy: Current knowledge

6k  Low eicosapentaenoic acid and gamma-linolenic acid levels in breast adipose tissue are associated with inflammatory breast cancer

Lifestyle modifications for patients with breast cancer to improve prognosis and optimize overall health.

8 Prolonged Nightly Fasting and Breast Cancer Prognosis

9 Diet-induced obesity links to ER positive breast cancer progression via LPA/PKD-1-CD36 signaling-mediated microvascular remodeling.

10 Triple-negative breast cancer and its association with obesity

Further reading:

Reexamining cancer metabolism: lactate production for carcinogenesis could be the purpose and explanation of the Warburg Effect

Out of Warburg effect: An effective cancer treatment targeting the tumour specific metabolism and disregulated pH.

Anti-Cancer Effect of Panax Ginseng and Its Metabolites: From Traditional Medicine to Modern Drug Discovery:

EMT Factors and metabolic pathways in cancer

Aerobic glycolysis and high level of lactate in cancer metabolism and microenvironment

Reexamining cancer metabolism: lactate production for carcinogenesis could be the purpose and explanation of the Warburg Effect

A New inhibitor of glucose-6-phosphate dehydrogenase blocks pentose photphate pathway and suppresses malignant proliferation and metastasis in vivo:

The effect of magnesium supplementation on lactate levels of sportsmen and sedanter.

Targeting Glutamine Metabolism for Cancer Treatment

Hypercalcemia in metastatic breast cancer unrelated to skeletal metastasis

Magnesium Supplementation in Vitamin D Deficiency.

Vitamin D, calcium homeostasis and aging
Proper Calcium Use: Vitamin K2 as a Promoter of Bone and Cardiovascular Health

Something more to say about calcium homeostasis: the role of vitamin K2 in vascular calcification and osteoporosis.

Ketones and lactate increase cancer cell “stemness”, driving recurrence, metastasis and poor clinical outcome in breast cancer

Lactate in the Regulation of Tumor Microenvironment and Therapeutic Approaches

Lactate Beyond A Waste Metabolite: Metabolic Affairs and Signaling in Malignancy

Achieving personalized medicine via metabolo-genomics

Natural anti-clotting foods

Berberine Suppresses Fibronectin Expression through Inhibition of c-Jun Phosphorylation in Breast Cancer Cells

Blocking Cancer With Combinations of Supplements and Off-Label Drugs

The Pentose Phosphate Pathway as a Potential Target for Cancer Therapy

Dehydroepiandrosterone sulfate causes proliferation of estrogen receptor–positive breast cancer cells despite treatment with fulvestrant

City of Hope Scientist Explores Genomic Instability as the Key Link Between Diabetes and Cancer

Disclaimer: I am not a medical professional. I do not claim that anything which worked for me would work the same for you. This blog is no substitute for the advice of your doctor. Always seek medical advice if you have any concerns. Always check with your consultant before taking any supplements. This blog is my personal journey and a journal of how I coped. I do not take any financial incentives from any products mentioned.