Practical takeaways from the paper
“Dietary factors and their influence on immunotherapy strategies in oncology: a comprehensive review”

(Cell Death & Disease, 2024).
https://www.nature.com/articles/s41419-024-06641-6

The review is an impressively thorough and forward-thinking synthesis that bridges nutritional science, immunology and oncology, offering clinicians a clear map of how specific diets and nutrients can modulate checkpoint-blockade outcomes. Its careful balance of mechanistic detail with practical implications makes it a valuable reference for researchers and frontline practitioners.

Heartfelt thanks to the authors for their meticulous scholarship and for advancing a conversation that holds real promise for improving patient care.

Practical takeaways of note for patients:

1. Dietary Patterns Influencing Immunotherapy

• A Western, ultra-processed diet is pro-inflammatory and can undermine immune-checkpoint inhibitor (ICI) efficacy.
  
• Mediterranean-style, fibre-rich eating supports an anti-inflammatory milieu and a gut microbiome profile associated with better ICI response.

2. Fibre and Short-Chain Fatty Acids

• High dietary fibre increases short-chain fatty acids such as butyrate production, which expand regulatory T-cells and correlate with improved PD-1/PD-L1 therapy outcomes in pre-clinical models.

3. Ketogenic Diet (KD)

• Mouse studies show KD raises CD4⁺ T-cell counts, shrinks tumours and potentiates anti-PD-1 therapy; the benefit disappears if T-cells are depleted.
  
• 3-hydroxybutyrate (a primary ketone body) itself can retard tumour growth and prevent PD-L1 up-regulation tied to immune escape.
  

4. Low-Protein / Methionine-Restricted Diets

• In lymphoma, melanoma and colorectal cancer models, a low-protein diet slows tumour growth only when CD8⁺ T-cells are intact, indicating synergy with immunosurveillance and ICIs.
  
• Methionine restriction up-regulates MHC-I and PD-L1 on tumour cells, potentially heightening antigen presentation and augmenting ICI activity.
  

5. Caloric Restriction & Fasting-Mimicking Diets

• Short-term fasting or caloric restriction enhances anti-PD-1/PD-L1 antibodies when combined with agents that induce immunogenic cell death, mainly by facilitating extracellular ATP release that sparks innate immunity.
  

6. Gut Microbiome Modulation

• Broad-spectrum antibiotics abolish CTLA-4 and PD-1 efficacy in mice; recolonising with specific species such as Bifidobacterium restores response, underscoring diet–microbiome–ICI interactions.
  

7. Vitamin D

• Retrospective data in melanoma patients: taking ≥1,000 IU/day before starting ICIs significantly lowers the odds of developing ICI-induced colitis in a dose-dependent manner.
  

8. Vitamin C

• Intravenous high-dose vitamin C (15–25 g) can raise blood antioxidant capacity and reduce chemotherapy toxicity, but doses >25 g have the opposite effect; evidence for direct immunotherapy synergy is lacking.
  

9. Dairy Whey Proteins & Lactoferrin

• Whey protein concentrate supplying ≥40% of daily protein needs shortened the duration of chemotherapy-induced oral mucositis in stem-cell transplant patients; lactoferrin exhibits immunomodulatory and anticancer properties in pre-clinical studies.

https://www.nature.com/articles/s41419-024-06641-6/figures/5

Summary of Dietary Impacts
↑ = increase    ↓ = decrease

High-Fibre Diet

• Short-chain fatty acids (SCFAs) ↑
  
• ATP release in the gut ↑
  
• T-cell expansion ↑
  
• Interferon-γ (IFN-γ) secretion

Ketogenic / High-Fat, Low-Carb Diet

• Blood glucose ↓
  
• Lactate production ↓ → dendritic-cell maturation ↑ → NK-cell activation ↑ → CD4⁺ T-cell population ↑
  
• 3-Hydroxybutyrate ↑ → PD-L1 expression ↑ via EGFR/ERK/c-Jun signaling
  
• Pro-inflammatory cytokine release ↑ (systemic inflammation ↑)
  

C. Low-Protein / Methionine-Restricted Diet

• IRE1α pathway activation ↑
  
• RIG-I pathway activation ↑ → cytokine release ↑
  
• Methionine availability ↓
  
• Cancer-cell MHC-I and PD-L1 surface expression ↑
  
• M1-type macrophages ↑, M2-type macrophages ↓

D. Caloric Restriction (10–50% Energy Cut)

• Circulating substrates (insulin, glucose, TNF-α, VEGF, IL-6) ↓
  
• Ketone bodies ↑
  
• Tumour desmoplasia ↓, regulatory T-cells ↓, overall inflammation ↓, cytotoxic T-cells ↑
  
• Cancer-cell Akt/mTOR signaling ↑, autophagy ↑, RAS/MAPK signaling ↑,
  senescence ↑
  
• Result: cancer cells become more sensitive to antimitotic agents; improved drug delivery and tumour clearance in the microenvironment.
  

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