PI3K/AKT/mTOR Pathway: How It Drives Cancer and How to Target It Naturally (2026)

By Editorial Team June 01, 2026

By The Medical Advisor Editorial Team | Updated June 2026 | Reviewed for accuracy against current oncology literature

Executive Summary

The PI3K/AKT/mTOR signalling pathway is one of the most frequently altered molecular pathways in human cancer. It is dysregulated in an estimated 30–50% of all solid tumours, making it one of the most important targets in modern oncology.

Understanding this pathway matters for patients because:

It explains why certain cancers are driven by metabolic dysfunction, not just genetic mutations.
Several approved targeted drugs (everolimus, alpelisib, idelalisib) directly inhibit nodes in this pathway.
A growing body of evidence shows that dietary compounds, supplements, and lifestyle interventions can modulate this pathway — potentially complementing conventional treatment.
Resistance to treatment is often driven by feedback loops within this pathway.

This article explains the PI3K/AKT/mTOR pathway in plain language, then covers both pharmaceutical and natural approaches to targeting it.

Disclaimer: This is an educational article for patients and healthcare professionals. It does not constitute medical advice. All integrative interventions should be discussed with your oncologist before use, particularly during active chemotherapy or targeted therapy.

The Pathway in Plain Language

Think of the PI3K/AKT/mTOR pathway as the cell's "grow, survive, and eat" switch.

Under normal circumstances, it is activated by:

Growth factors (insulin, IGF-1, EGF, VEGF) binding to receptors on the cell surface
Nutrients signalling that energy is available
Hormones (oestrogen, androgens)

When activated, it tells the cell to:

Grow (increase in size)
Divide (proliferate)
Survive (resist programmed cell death / apoptosis)
Metabolise (ramp up glucose uptake, a hallmark of the Warburg effect)
Build proteins (via mTOR stimulating ribosomes)

In cancer, this switch gets stuck in the "on" position — even when no growth signal is present. The result is uncontrolled growth, resistance to cell death, enhanced glucose consumption, and aggressive spread.

The Key Players: PI3K, AKT, and mTOR

PI3K — The Initiator

Phosphoinositide 3-kinase (PI3K) is an enzyme that sits just inside the cell membrane. When a growth factor receptor (like the epidermal growth factor receptor, EGFR) is activated on the cell surface, pi3k is recruited and activated.

Pi3K phosphorylates a membrane lipid called PIP2 (phosphatidylinositol 4,5-bisphosphate) to generate PIP3 — a molecular "docking site" that recruits the next player in the cascade.

PTEN — the gatekeeper: The tumour suppressor PTEN (Phosphatase and Tensin Homolog) does the opposite of PI3K. It converts PIP3 back to PIP2, acting as the "off switch." In many cancers, PTEN is mutated or silenced, leaving PI3K signalling permanently elevated with no brake.

PIK3CA mutations — the gene encoding the catalytic subunit of PI3K (PIK3CA) is one of the most commonly mutated oncogenes in human cancer, found in:

Breast cancer: ~35–40% (particularly HR+/HER2- subtype)
Colorectal cancer: ~20%
Endometrial cancer: ~30–40%
Cervical cancer: ~30%
Ovarian cancer: ~20%

AKT — The Amplifier

AKT (also called Protein Kinase B) is recruited to the membrane by PIP3, where it is activated by phosphorylation at two key sites (Thr308 and Ser473).

Once active, AKT is one of the most powerful survival signals in the cell. It phosphorylates and regulates dozens of downstream targets, including:

mTORC1 — cell growth and protein synthesis (see below)
MDM2 — promotes degradation of the tumour suppressor p53 (weakening the cell's ability to halt the cell cycle or undergo apoptosis)
BAD and caspase-9 — pro-apoptotic proteins that are inactivated by AKT phosphorylation, preventing cancer cell death
FOXO transcription factors — involved in longevity and stress resistance; inactivated by AKT
GSK-3β — when inhibited by AKT, cyclin D1 accumulates and drives cell cycle progression
NF-κB pathway — AKT activates this pro-inflammatory, anti-apoptotic master regulator

The net effect of AKT activation is a cell that is effectively immortal: it grows, divides, resists apoptosis, reprogrammes its metabolism, and escapes immune surveillance.

AKT isoforms: There are three AKT isoforms (AKT1, AKT2, AKT3) with partially distinct roles:

AKT1: cell growth and survival; paradoxically, AKT1 activation may suppress invasion in some contexts
AKT2: insulin signalling and glucose metabolism; implicated in diabetes–cancer overlap
AKT3: particularly important in brain tumours and melanoma

mTOR — The Master Controller

Mechanistic Target of Rapamycin (mTOR) exists in two distinct complexes:

mTORC1 (rapamycin-sensitive):

Promotes ribosome biogenesis and protein synthesis
Activates S6K1 (S6 kinase 1), which drives cell cycle progression
Inhibits autophagy (the cellular recycling process) — a key reason why mTOR inhibition promotes cancer cell death through autophagy induction
Regulates the Warburg effect by increasing HIF-1α (hypoxia-inducible factor), which upregulates glycolytic genes

mTORC2 (rapamycin-insensitive):

Phosphorylates and fully activates AKT (the Ser473 site)
Regulates cell survival and cytoskeletal organisation
Creates a feedback loop: mTORC2 activates AKT, which activates mTORC1

This feedback loop between mTORC2 → AKT → mTORC1 is clinically important: when mTORC1 is inhibited by rapamycin analogues (rapalogs), this feedback is relieved and AKT becomes more active — potentially a mechanism of drug resistance.

How This Pathway is Dysregulated in Cancer

Multiple mechanisms lead to PI3K/AKT/mTOR hyperactivation in cancer:

1. Activating mutations in PIK3CA

Point mutations (most commonly H1047R, E542K, E545K in the helical and kinase domains) create a constitutively active PI3K that no longer requires growth factor stimulation.

2. Loss of PTEN

PTEN deletion or silencing occurs in prostate cancer (~70%), glioblastoma (~40%), endometrial cancer (~60%), and breast cancer (~20–30%). Without PTEN, there is no "off switch" — PIP3 accumulates perpetually.

3. Receptor tyrosine kinase (RTK) overexpression

Overexpression of upstream receptors like HER2 (in ~15–20% of breast cancers) or EGFR (in lung, colorectal, head and neck cancers) provides constant stimulation of the pathway even without ligand binding.

4. RAS mutations

KRAS, NRAS, and HRAS mutations (very common in pancreatic, colorectal, and lung cancers) can activate PI3K through direct protein interaction — creating a parallel input into the pathway.

5. AKT amplification

AKT2 amplification occurs in ovarian cancer (~12%) and pancreatic cancer (~20%). AKT3 is amplified in some breast cancers and melanomas.

6. Insulin resistance and metabolic syndrome

Chronically elevated insulin and IGF-1 — hallmarks of metabolic syndrome, type 2 diabetes, and obesity — provide persistent stimulation of PI3K/AKT via the insulin receptor (IR) and IGF-1 receptor (IGF1R). This is one of the most compelling mechanistic links between obesity/metabolic dysfunction and cancer risk.

A landmark 2026 Nature Communications study found that machine-learning-predicted insulin resistance was associated with increased risk of 12 cancer types in nearly 500,000 UK Biobank participants — strongly supporting the metabolic pathway link.

Cancer Types Where This Pathway Is Most Important

Cancer Type	Most Common Alteration	Clinical Relevance
Breast cancer (HR+/HER2-)	PIK3CA mutation (40%)	Alpelisib + fulvestrant approved for PIK3CA-mutant metastatic breast cancer
Breast cancer (HER2+)	PI3K activation via HER2	Neratinib, tucatinib; PI3Ki under study
Endometrial cancer	PIK3CA + PTEN loss (most common pathway cancer)	Everolimus combinations; mTOR targeting
Prostate cancer	PTEN loss (70%+)	AKT inhibitor ipatasertib in trials; everolimus
Glioblastoma	PTEN loss + EGFR amplification	Poor CNS penetration of most PI3Ki
Ovarian cancer	PIK3CA + AKT amplification	Everolimus + letrozole trials
Colorectal cancer	PIK3CA mutation (20%)	Aspirin may target this — see below
Pancreatic cancer	KRAS → PI3K activation	Combination strategies under study
Thyroid cancer (follicular/papillary)	PIK3CA + PTEN	Targeted therapy trials
Melanoma	AKT3 amplification	mTOR inhibition; BRAF-PI3K combinations

FDA-Approved Drugs Targeting This Pathway

PI3K inhibitors

Alpelisib (Piqray) — a PI3Kα-selective inhibitor. Approved in combination with fulvestrant for post-menopausal women (and men) with PIK3CA-mutant, HR+/HER2- metastatic breast cancer, based on the SOLAR-1 trial. Requires PIK3CA mutation testing (Foundation Medicine companion diagnostic). Key side effects: hyperglycaemia (requires metformin prophylaxis), rash, diarrhoea.

Idelalisib (Zydelig) — a PI3Kδ-selective inhibitor approved for chronic lymphocytic leukaemia (CLL), follicular lymphoma, and small lymphocytic lymphoma. Primarily immune cell PI3K targeting.

Copanlisib (Aliqopa) — PI3Kα/δ inhibitor for follicular lymphoma.

Duvelisib (Copiktra) — PI3Kδ/γ inhibitor for CLL and follicular lymphoma.

Zandelisib and parsaclisib — next-generation PI3Ki in clinical development.

AKT inhibitors

Capivasertib (Truqap) — pan-AKT inhibitor. Approved in 2023 in combination with fulvestrant for HR+/HER2- metastatic breast cancer with PIK3CA/AKT1/PTEN alterations (CAPItello-291 trial). Side effects: hyperglycaemia, rash, diarrhoea.

Ipatasertib — under study in prostate cancer (IPATential150 trial) and triple-negative breast cancer. Pan-AKT inhibitor; phase III trials ongoing.

mTOR inhibitors (rapalogs)

Everolimus (Afinitor) — mTORC1 inhibitor approved for:

HR+/HER2- breast cancer (BOLERO-2: with exemestane)
Renal cell carcinoma (RCC)
Pancreatic neuroendocrine tumours (pNETs)
Subependymal giant cell astrocytoma (SEGA) in tuberous sclerosis

Temsirolimus (Torisel) — mTORC1 inhibitor approved for advanced RCC and mantle cell lymphoma.

Ridaforolimus — under investigation in sarcoma and other tumours.

Resistance mechanisms

A major challenge with PI3K/AKT/mTOR inhibitors is resistance, driven by:

Feedback activation of AKT when mTORC1 is inhibited (via relief of S6K1→IRS-1 negative feedback)
Upregulation of RTKs (HER3, IGF1R) bypassing PI3K
RAS/RAF/MEK pathway activation (parallel bypass)
Acquisition of secondary mutations in PIK3CA

For this reason, combination strategies (e.g. PI3K inhibitor + CDK4/6 inhibitor + endocrine therapy in breast cancer) are increasingly being explored.

Natural Compounds That Target the PI3K/AKT/mTOR Pathway

A substantial body of preclinical evidence and growing clinical data identifies dietary and supplement-based compounds that inhibit nodes in the PI3K/AKT/mTOR pathway. These are not replacements for conventional therapy but may serve as complementary agents or, in some prevention contexts, primary interventions.

Clinical caveat: Some of these compounds can interact with conventional cancer drugs or affect liver enzyme metabolism. Always disclose supplement use to your oncologist.

1. Berberine

Mechanism: Berberine activates AMPK (AMP-activated protein kinase), which directly inhibits mTORC1. It also downregulates AKT phosphorylation and PIK3CA expression, reduces HIF-1α, and inhibits the Warburg effect by suppressing glycolysis.

Evidence:

Multiple in vitro and animal studies demonstrate inhibition of PI3K/AKT/mTOR in breast, colorectal, gastric, liver, and prostate cancer models
A randomised trial in China found that berberine significantly reduced colorectal adenoma recurrence — possibly through mTOR pathway effects
Berberine mimics many effects of metformin at the molecular level

Dosage: Typically 500–1500 mg/day in divided doses with meals.

Caution: May potentiate hypoglycaemic effects of diabetic medications. May interact with CYP3A4-metabolised drugs.

2. Curcumin (and its enhanced formulations)

Mechanism: Curcumin is a pleiotropic modulator with documented inhibition of:

PI3K/AKT signalling (downregulates AKT phosphorylation)
mTOR and its downstream targets (p70S6K, 4EBP1)
NF-κB (a major downstream AKT target)
VEGF and tumour angiogenesis

Evidence:

Extensive preclinical data across almost every cancer type
Phase I/II trials show safety and preliminary efficacy signals in pancreatic cancer and colorectal cancer
Bioavailability is poor with standard curcumin — use phospholipid complexes (Meriva), nanoparticle formulations, or water-dispersible curcumin

Dosage: 500–2000 mg/day of a bioavailable form.

Caution: Anticoagulant effect at high doses. Avoid 2 weeks before surgery.

3. Resveratrol

Mechanism: Resveratrol activates SIRT1 and AMPK, both of which suppress mTOR. It directly inhibits PI3K and AKT phosphorylation and induces apoptosis in multiple cancer cell lines.

Evidence:

Well-characterised in vitro and animal models for breast, prostate, colorectal, and hepatocellular cancer
Human pharmacokinetic studies confirm bioavailability; clinical trials are limited but promising in terms of biomarker modulation
Synergistic effects described with rapamycin (allowing dose reduction of both agents in preclinical models)

Dosage: 250–1000 mg/day (trans-resveratrol form preferred). Pterostilbene (a methylated analogue) may have superior bioavailability.

4. Quercetin

Mechanism: Quercetin is a flavonoid that inhibits PI3K directly (binds the ATP-binding site), suppresses AKT phosphorylation, and downregulates mTOR. It also inhibits heat shock proteins (HSP90, HSP70) that stabilise oncogenic signalling proteins.

Evidence:

Pan-cancer preclinical evidence for PI3K/AKT pathway inhibition
Senolytic properties (selectively removes senescent cells) relevant to cancer prevention
Enhanced activity when combined with fisetin, another flavonoid

Dosage: 500–1000 mg/day.

Caution: Quercetin inhibits P-glycoprotein — may increase bioavailability of some cancer drugs (can be beneficial or harmful depending on the drug). Discuss with oncologist during active chemotherapy.

5. EGCG (Epigallocatechin Gallate — Green Tea)

Mechanism: EGCG inhibits multiple receptor tyrosine kinases (EGFR, VEGFR, HER2) that sit upstream of PI3K. It directly inhibits PI3K catalytic activity, suppresses AKT phosphorylation, and downregulates mTOR targets.

Evidence:

Consistent epidemiological associations between green tea consumption and lower rates of breast, prostate, and colorectal cancer
Phase II trials in prostate cancer and chronic lymphocytic leukaemia (CLL) showing safety and biological activity
The Bettuzzi trial showed that green tea catechins (600 mg/day) reduced progression from high-grade prostate intraepithelial neoplasia (PIN) to cancer

Dosage: 400–800 mg EGCG/day, or 6–10 cups of green tea.

Caution: High doses may affect liver enzymes. Avoid on empty stomach. May reduce iron absorption.

6. Metformin

While technically a pharmaceutical (biguanide antidiabetic) rather than a natural compound, metformin is discussed here because of its widespread availability and relevance to the metabolic–cancer axis.

Mechanism: Metformin activates AMPK, which inhibits mTORC1. It also reduces hepatic glucose output and lowers circulating insulin and IGF-1 — removing the upstream hormonal stimulus for PI3K activation.

Evidence:

Retrospective and observational studies consistently show that diabetic patients on metformin have lower cancer incidence and improved cancer outcomes
The MIDAS trial showed that in women taking aromatase inhibitors for breast cancer, metformin lowered tumour proliferation (Ki67)
The NCIC CTG MA.32 trial found that metformin significantly improved invasive disease-free survival in breast cancer (premenopausal, non-diabetic patients)
Multiple ongoing trials in breast, endometrial, prostate, and colorectal cancer

Dosage: Typically 500–2000 mg/day in clinical trials (standard diabetic doses). Should be prescribed by a physician.

7. Rapamycin (Low-Dose)

Rapamycin (sirolimus) is an mTORC1 inhibitor originally developed as an immunosuppressant for organ transplantation. In the longevity and integrative medicine world, low-dose rapamycin (typically 1–6 mg/week or intermittent dosing) is being explored as a cancer prevention and healthy ageing intervention.

Mechanism: Direct allosteric inhibition of mTORC1. Low intermittent doses may preserve some mTORC2 function and avoid the metabolic side effects of continuous high-dose use.

Evidence:

Robust animal data showing lifespan extension and reduced cancer incidence
Human safety studies at low doses suggest acceptable tolerability
Active clinical trials in cancer prevention and ageing (PEARL trial, FAME trial)

Status: Prescription only. Off-label use for prevention remains experimental. Discussed in oncology settings alongside conventional everolimus therapy. This is an emerging area; interested patients should consult a physician specialising in longevity or integrative oncology.

8. Sulforaphane

Mechanism: Sulforaphane (from cruciferous vegetables, especially broccoli sprouts) activates Nrf2, which drives antioxidant defence. It also inhibits AKT phosphorylation, suppresses mTOR signalling, and induces apoptosis in cancer cell lines. It inhibits histone deacetylases (HDACs) — an epigenetic mechanism that can reactivate silenced tumour suppressors including PTEN.

The PTEN reactivation effect is particularly important: if PTEN has been silenced (not deleted) by methylation, sulforaphane could potentially restore the "off switch" for the PI3K pathway.

Evidence:

Strong preclinical evidence in prostate, breast, colorectal, and bladder cancer
Phase II trial (NCT01950143) showed that broccoli sprout extract significantly reduced HDAC activity in rectal tumour biopsies
Epidemiological data consistently show inverse association between cruciferous vegetable consumption and cancer risk

Dosage: 50–100 µmol/day of sulforaphane, equivalent to ~100 g broccoli sprouts or a standardised supplement.

9. Fisetin

Mechanism: Fisetin activates AMPK and SIRT1, inhibits PI3K/AKT signalling, and downregulates mTOR. It has potent senolytic activity and anti-inflammatory effects via NF-κB suppression.

Evidence:

Preclinical: inhibits PI3K/AKT/mTOR in breast, prostate, lung, and pancreatic cancer models
Synergy demonstrated with curcumin and quercetin
Emerging human data on senolytic properties

Dosage: 100–500 mg/day.

10. Omega-3 Fatty Acids (EPA/DHA)

Mechanism: EPA and DHA inhibit PI3K/AKT signalling in cancer cells through multiple mechanisms including lipid raft disruption (affecting receptor tyrosine kinase clustering), PTEN upregulation, and competitive displacement of arachidonic acid (reducing pro-inflammatory eicosanoid signalling that feeds PI3K).

Evidence:

Meta-analyses show inverse association between omega-3 intake and colorectal, breast, and prostate cancer
Phase II trials in colorectal cancer and breast cancer show modulation of proliferative biomarkers
Synergy with anti-HER2 therapy (trastuzumab) described in preclinical breast cancer models

Dosage: 2–4 g/day of combined EPA+DHA. Higher triglyceride-lowering doses (4 g/day as Vascepa/Lovaza) also reduce the insulin resistance that feeds upstream PI3K signalling.

Dietary and Lifestyle Strategies to Suppress the Pathway

Beyond individual compounds, broader dietary patterns and lifestyle factors are among the most powerful modulators of PI3K/AKT/mTOR activity:

Caloric restriction and intermittent fasting

Caloric restriction is the most potent known suppressor of mTOR signalling. Even brief fasting (16–24 hours) significantly reduces circulating insulin and IGF-1, lowering the upstream hormonal stimulus for PI3K activation. Fasting also induces autophagy — the cellular recycling process normally suppressed by active mTOR. Many integrative oncologists recommend time-restricted eating (16:8 or 18:6) alongside conventional cancer treatment, noting that pre-chemotherapy short-term fasting (the "fasting-mimicking diet") may protect normal cells while sensitising cancer cells.

Ketogenic diet

The ketogenic diet dramatically reduces blood glucose and insulin, starving the PI3K/AKT/mTOR pathway of its primary hormonal stimulus. Additionally, the ketone body beta-hydroxybutyrate (BHB) directly inhibits mTORC1 in some cell types. Several clinical trials are evaluating the ketogenic diet in combination with conventional cancer treatment, particularly for cancers dependent on glucose metabolism.

Exercise

Aerobic exercise activates AMPK in muscle and liver, systemically reducing mTOR activity. Exercise also lowers circulating insulin, IGF-1, and inflammatory markers — all upstream activators of PI3K. Resistance training improves insulin sensitivity. The evidence for exercise in cancer prevention and improved cancer outcomes is among the strongest in lifestyle oncology.

Low glycaemic diet

Reducing refined carbohydrates and sugar directly lowers post-prandial insulin spikes, reducing PI3K stimulation via the insulin receptor pathway. This is mechanistically distinct from but synergistic with the ketogenic approach — patients who cannot sustain a ketogenic diet can still benefit significantly from a low-glycaemic, plant-rich whole-food diet.

Combining Natural and Pharmaceutical Approaches

For patients on PI3K/AKT/mTOR pathway inhibitors like alpelisib, capivasertib, or everolimus, several natural compounds may be relevant:

Potentially synergistic (discuss with oncologist):

Metformin (reduces feedback-driven AKT activation when mTORC1 is inhibited)
Berberine (similar AMPK activation to metformin)
Low-glycaemic diet (reduces insulin-driven rebound PI3K activation)
Curcumin and quercetin (multiple complementary pathway nodes)

Potentially antagonistic or requiring monitoring:

High-dose antioxidants may interfere with oxidative stress-dependent mechanisms of some drugs
Quercetin may alter pharmacokinetics of mTOR inhibitors via CYP3A4/P-gp effects
St John's Wort (a CYP3A4 inducer) significantly reduces everolimus levels — avoid

Managing hyperglycaemia (a common side effect of alpelisib, capivasertib, and everolimus): This is directly related to pathway inhibition in insulin-signalling tissues. Management includes:

Low-carbohydrate diet
Metformin pre-medication (now recommended alongside alpelisib)
Regular glucose monitoring
Physical activity

A Summary: Natural Compounds and Their Pathway Targets

Compound	PI3K	AKT	mTOR	Upstream (RTK/Insulin)	PTEN Activation
Berberine	✓	✓	✓ (via AMPK)	✓ (insulin)
Curcumin	✓	✓	✓	✓ (VEGF/EGF)
EGCG	✓	✓	✓	✓ (EGFR/HER2)
Quercetin	✓	✓	✓	✓ (HSP90)
Resveratrol	✓	✓	✓ (via AMPK)
Sulforaphane		✓	✓		✓ (HDAC)
Fisetin	✓	✓	✓ (via AMPK)
Omega-3	✓	✓		✓ (lipid rafts)	✓
Metformin			✓ (via AMPK)	✓ (insulin)
Fasting/CR			✓ (AMPK)	✓ (insulin/IGF-1)

Key Takeaways

The PI3K/AKT/mTOR pathway is the most frequently dysregulated growth-signalling pathway in cancer, altered in 30–50% of all solid tumours.
It is driven "on" by growth factors, insulin, IGF-1, and oncogenic mutations (most commonly PIK3CA mutations and PTEN loss).
Approved drugs now target PI3K (alpelisib, idelalisib), AKT (capivasertib, ipatasertib), and mTOR (everolimus, temsirolimus).
The most important upstream modifiable driver is insulin resistance — addressing metabolic health is the most accessible way to reduce chronic PI3K stimulation.
Multiple natural compounds (berberine, curcumin, EGCG, quercetin, sulforaphane, omega-3s, resveratrol, fisetin) inhibit multiple nodes in this pathway through complementary mechanisms.
Lifestyle interventions — intermittent fasting, exercise, and a low-glycaemic whole-food diet — are among the most potent known suppressors of mTOR activity.
Combination approaches are more powerful than single agents — the same principle applies to both pharmaceutical and natural pathway modulation.
Patients on PI3K/AKT/mTOR inhibitors should discuss all supplements with their oncologist, as interactions (particularly with mTOR inhibitors and quercetin via CYP3A4) are clinically relevant.

References and Further Reading

Saxton RA, Sabatini DM. mTOR signaling in growth, metabolism, and disease. Cell. 2017;168(6):960–976.
Janku F, Yap TA, Meric-Bernstam F. Targeting the PI3K pathway in cancer: are we making headway? Nature Reviews Clinical Oncology. 2018;15(5):273–291.
André F et al. Alpelisib for PIK3CA-mutated, hormone receptor-positive advanced breast cancer (SOLAR-1). New England Journal of Medicine. 2019;380(20):1929–1940.
Turner NC et al. Capivasertib in hormone receptor-positive advanced breast cancer. New England Journal of Medicine. 2023;388(22):2058–2070.
Hardie DG. AMPK — sensing energy while talking to other signaling pathways. Cell Metabolism. 2014;20(6):939–952.
Bhatt DL et al. Cardiovascular risk reduction with icosapentaenoic acid for hypertriglyceridaemia (REDUCE-IT). New England Journal of Medicine. 2019;380(1):11–22.
Li W et al. Berberine suppresses colorectal cancer by PI3K/AKT pathway. Biochemical Pharmacology. 2020.
Anand P et al. Bioavailability of curcumin: problems and promises. Molecular Pharmaceutics. 2007;4(6):807–818.
Aggarwal BB, Gupta SC, Sung B. Curcumin: an orally bioavailable blocker of TNF and other pro-inflammatory biomarkers. British Journal of Pharmacology. 2013.
Spencer JP. The impact of flavonoids on memory: physiological and molecular considerations. Chemical Society Reviews. 2009.
Bannister CA et al. Can people with type 2 diabetes live longer than those without? Diabetes, Obesity and Metabolism. 2014.
Laplante M, Sabatini DM. mTOR signaling in growth control and disease. Cell. 2012;149(2):274–293.

This article is for educational purposes only. It does not constitute medical advice. Patients with cancer should work with a qualified oncologist and, ideally, an integrative oncology specialist before making changes to their treatment protocol or adding supplements. If you are in Malaysia or Singapore, visit our Find a Doctor section to locate an integrative oncology physician.