Diet and Cancer, Part 2: How Nutrition Shapes Tumor Metabolism

Dietary Interventions in Cancer

This is the Second of a two part series “What to eat when you have cancer.” Dietary interventions are central to the metabolic management of cancer. You are what you eat.

The Glycemic Index

The glycemic index is a value assigned to food based on how quickly those foods cause increases in blood glucose levels and how high they spike (see figure 1). The glycemic index ranks food on a scale from 0 to 100. Pure glucose is arbitrarily given a value of 100, which represents the relative rise in the blood glucose level after two hours. The glycemic index of a specific food depends primarily on the quantity and type of carbohydrate it contains (see Table 1). Foods that are low on the glycemic index (GI) scale tend to release glucose slowly and steadily. Foods that are high on the glycemic index release glucose rapidly. It should be noted that the glycemic index varies between individuals. (1, 2) A CGM allows for the individual assessment of the glucose excursion (glycemic index) of various foods.

Figure 1. The blood glucose profiles of a high and low glycemic index food.

What to eat and what not to eat!

The most important intervention to reduce obesity, metabolic syndrome, type II diabetes, cancer, cardiac disease, neurodegenerative diseases, autoimmune diseases etc., is to eat real food and not processed food. (3-5) Telling the difference is quite simple. If it looks like food, it is real. If it comes in a box or has a food label, it’s likely processed. The more ingredients listed on a product’s label and the more chemicals you see with strange and unpronounceable names, the more processing the product has undergone. Recent evidence suggests that processed foods in themselves can cause insulin resistance. (6)

Healthy foods include:

• All vegetables (especially avocados, and cruciferous and leafy vegetables)

• Nuts (almonds, Brazil nuts, cashews, and pistachios)

• Peanut butter (but avoid the white bread and grape jelly!) and chia seeds

• Fish (wild fresh fish especially Alaskan/Pacific salmon and sardines)

• Chicken breast (free range, no hormones, no antibiotics)

• Eggs (they’ve been giving a bad rap!); free range “organic” eggs are suggested

• Meat (grass-fed, no hormones, avoid processed meats)

• Blueberries (limit volume if insulin resistant)

• Coffee with heavy cream or coconut oil; choose Stevia (without erythritol) over sugar or artificial sweeteners.

What not to eat!

• Donuts, bagels, bread, pretzels, tortillas

• Cookies, muffins, baked goods

• Fries, chips

• Rice and pasta

• Potatoes

• Canned fruit and fruit juice

• Sweetened yogurt

• Watermelon, bananas

Figure 2. What to eat!

Figure 3. What not to eat!

Flattening the glucose curve

Apart from carbohydrate restriction/ketogenic diet and time-restricted eating, several simple interventions (or hacks) prevent the high glucose spikes that fuel cancer. The book “Glucose Revolution” by Jessie Inchauspe is highly recommended and provides more details on interventions to flatten the blood glucose curve, such as. (7)

Eat foods in the right order

Veggies (greens/fiber) should be eaten first, protein and fat second, and starch (sugars) last; this slows gastric emptying, as well as the breakdown and absorption of glucose. Eat fruit last; always preceded by fiber. Don’t begin a meal with bread (starch).

• Begin a meal with a salad or green vegetables. Use olive oil and vinegar as salad dressing.

• Avoid starchy foods with no fiber.

• Avoid fruit juices and smoothies, which cause a large glucose spike.

• Skip breakfast. Breakfast is the worst time to eat sugar and starches; this results in a large glucose spike. Cereal for breakfast causes a rapid spike in glucose.

• Avoid snacking throughout the day.

• Drink a tablespoon of vinegar stirred into a tall glass of water before eating starch or something sweet. Apple cider vinegar is recommended. The acetic acid in vinegar decreases the enzymatic breakdown of starch, increases glycogen synthesis (and glucose uptake), and increases fatty acid oxidation. (8-11) Vinegar may be beneficial even if consumed up to 20 minutes after a starchy food. Apple cider vinegar is usually unpasteurized and should be avoided in pregnancy. If vinegar is not readily available, consume a few fiber tablets (esp. glucomannan tablets) before eating a starchy/sweet treat.

Intermittent Fasting, Autophagy, and Cancer

Fasting has a profound effect on promoting immune system homeostasis, improving mitochondrial health, and increasing stem cell production. (12-16) It stimulates the clearance of damaged mitochondria (mitophagy), misfolded and foreign proteins, and damaged cells (autophagy). Intermittent fasting or time-restricted eating is the single most effective method to activate autophagy.

During autophagy, cytoplasmic constituents—including damaged, misfolded, and foreign proteins—are engulfed within double-membrane vesicles called autophagosomes. These autophagosomes then fuse with lysosomes to form autolysosomes, where the contents are degraded and recycled. Autophagy occurs at basal levels under normal physiological conditions and can be upregulated in response to various cellular stressors, including hypoxia, nutrient deprivation, DNA damage, and cytotoxic agents. (17) The molecular machinery regulating autophagy is evolutionarily conserved in higher eukaryotes and governed by specific ATG genes first characterized in yeast. The process of macroautophagy can also lead to cell death—referred to as “autophagic cell death”—due to the accumulation of autophagosomes and autolysosomes in the cytoplasm. Although the relationship between fasting, autophagy, and cancer is still being explored, many researchers propose that intermittent fasting may support the treatment and eradication of tumors and cancer cells. (18)

The metabolic effects of intermittent fasting are numerous and include increased insulin sensitivity; reductions in blood glucose, insulin, and IGF-1; activation of the sirtuin pathway; and stimulation of autophagy. Intermittent fasting is the most effective known strategy to activate autophagy and likely accounts for many of its therapeutic effects, especially in patients with cancer.

Although autophagy could theoretically support cancer cell proliferation, multiple studies have demonstrated that it more often leads to cancer cell death. (19) Many repurposed drugs used in cancer treatment have been shown to enhance tumor cell death by activating the autophagy pathway.

A limited number of rodent and human studies have evaluated the independent effects of intermittent fasting or time-restricted eating in modulating cancer progression. In a postmenopausal breast cancer mouse model driven by a high-fat diet, intermittent fasting markedly inhibited tumor initiation, progression, and metastasis compared with mice fed ad libitum, even without calorie restriction or weight loss. (20) This protective effect was likely mediated, at least in part, by reduced insulin signaling, as systemic insulin infusion via implanted pumps reversed the fasting-induced anticancer benefits. (20) Additional animal models have demonstrated similar benefits of intermittent fasting on cancer progression. (21-23)

Figure 4. Benefits of intermittent fasting

Recent in vitro and in vivo studies have shown that intermittent fasting improves the chemotherapeutic response to multiple agents in models of glioma, neuroblastoma, melanoma, fibrosarcoma, breast cancer, colon cancer, pancreatic cancer, hepatocellular cancer, and lung cancer. (17) Fasting appears to enhance chemotherapy effectiveness through several mechanisms, including:

• Enhanced DNA repair in normal cells, but not in malignant cells

• Improved autophagy as a protective mechanism against organelle damage

• Promotion of apoptosis by increasing tumor cell susceptibility to apoptotic stimuli and reducing apoptosis-mediated damage in normal cells

• Reduction of regulatory T cells and enhanced stimulation of CD8+ cytotoxic T cells

Modulating autophagy for cancer treatment is a promising therapeutic approach currently under intense investigation. Intermittent and prolonged fasting show promising benefits for people with cancer, particularly for improving tolerance to chemotherapy, reducing some treatment‑related side effects, and potentially enhancing treatment efficacy, but high‑quality human data are still limited. Fasting‑mimicking and time‑restricted eating protocols appear feasible and generally safe in selected patients under medical supervision; however, they may be harmful in those who are underweight, frail, or at risk of malnutrition.

Fasting can downregulate growth‑promoting pathways such as insulin/IGF‑1 and mTOR, which may slow tumor cell proliferation and sensitize cancer cells to chemotherapy and radiotherapy. Normal cells enter a protected, low‑metabolic state, a phenomenon termed differential stress resistance, potentially reducing collateral damage from cytotoxic therapy. In preclinical models, fasting and fasting‑mimicking diets (FMDs) enhance DNA damage in tumor cells, reduce angiogenesis, alter amino‑acid availability in the tumor microenvironment, and may improve immune surveillance (for example, reprogramming natural killer cells).

Data from small human trials suggest that various intermittent fasting regimens may positively influence risk factors linked to poor breast cancer outcomes, such as impaired glucoregulation, chronic inflammation, obesity, and poor sleep. Experimental animal models and observational human studies support the hypothesis that a prolonged nightly fasting interval, also known as time-restricted eating, may reduce cancer risk and improve outcomes. Marinac et al. investigated whether the duration of nightly fasting predicted recurrence and mortality among women with early-stage breast cancer. (24) The study included 2,413 women without diabetes mellitus, aged 27 to 70 years at diagnosis, who participated in the prospective Women’s Healthy Eating and Living study. Fasting duration was estimated from 24-hour dietary recalls collected at baseline, year 1, and year 4. The mean fasting duration was 12.5 ± 1.7 hours per night. In repeated-measures Cox proportional hazards regression models, fasting for fewer than 13 hours per night was associated with a higher risk of breast cancer recurrence compared with fasting for 13 hours or more per night (HR 1.36; 95% CI, 1.05-1.76).

Small early‑phase trials and observational studies suggest that short intermittent fasting (e.g., 14–16 hours/day or 48‑hour windows around chemotherapy) can reduce nausea, fatigue, and weakness and improve perceived quality of life during chemotherapy. Time‑restricted eating appears feasible for many patients and may support weight and metabolic control during and after treatment, with preliminary signals for oncologic benefit. Alternate‑day or restricted‑eating regimens in prostate and other cancers have shown reductions in tumor amino‑acid pools and global protein synthesis in animal models, increasing sensitivity to systemic therapies, with ongoing trials extending these regimens to human patients on hormone therapy or chemotherapy.(25)

Alternate‑day or restricted‑eating regimens in prostate and other cancers have shown reductions in tumor amino‑acid pools and global protein synthesis in animal models, increasing sensitivity to systemic therapies, with ongoing trials extending these regimens to human patients on hormone therapy or chemotherapy.

Prolonged short‑term fasting (typically 46–96 hours encompassing the period before and after chemotherapy) has been associated with fewer chemotherapy‑related toxicities, including reduced hematologic and gastrointestinal side effects, and lower rates of grade II–IV toxicities in small cohorts. Some studies report preservation of lymphocyte counts and white‑cell lineage balance with 48–72‑hour fasting, suggesting protection of normal hematopoietic tissue during cytotoxic therapy.(26)

The MICROBIOME in Cancer and Establishing/Restoring a “Normal” Microbiome

The microbiome is the community of microorganisms—mainly bacteria, fungi, viruses, and other microbes—and all their genes that live together in a specific environment, such as the human gut, skin, or soil. In humans, these microbes help with digestion, train and modulate the immune system, protect against pathogens, and can influence metabolism and overall health.

The microbiome has a remarkable effect on blood sugar levels and insulin sensitivity. (27-33) Establishing a normal microbiome is important for regulating blood glucose levels and improving insulin sensitivity. Furthermore, alterations in the microbiome play an important role in both tumorigenesis and tumor propagation.

Microbiome in oncogenesis

Key pro‑tumorigenic mechanisms include:

• Direct genotoxicity: Certain bacteria (for example colibactin‑producing E. coli, Enterotoxigenic Bacteroides fragilis) generate genotoxins and ROS/RNI that induce DNA damage, mutagenesis, and alter DNA repair, promoting transformation.(34)

• Chronic inflammation: Microbial activation of TLR/NOD pathways drives persistent production of IL‑6, TNF, IL‑17, and other cytokines, supporting cancer stem cells, angiogenesis, and immunosuppressive myeloid populations.(35)

• Metabolic reprogramming: Microbial metabolites (secondary bile acids, TMAO, nitrosamines) alter epithelial proliferation, apoptosis, and oncogenic signaling, especially in liver and colorectal carcinogenesis.(36)

Organ‑specific examples

In colorectal cancer, tumor-associated communities are enriched for Fusobacterium nucleatum, colibactin‑positive E. coli, and B. fragilis, which promote Wnt signaling, immune evasion, and metastatic behavior, while SCFA-producing commensals are often depleted. Colorectal cancer (CRC) patients exhibit distinct gut microbiota disruption known as dysbiosis which is believed to play a causative role in CRC. One of the key bacterial species implicated in CRC dysbiosis is Bacteroides fragilis, which presents a paradox as it is also present in most health individuals, The discrepancy underscores the need for analysis beyond species-level associations and to investigate intraspecies variation within B. fragilis. This line of research is exactly what is what Damgaard, et al performed and found a district bacteriophage (Caudoviricetes prophage) in that Bacteroides fragilis of those patients with cancer. (37) These findings suggest a partnership between bacteria and their viruses that may shape disease. If confirmed, these findings may support earlier detection of colorectal cancer and guide new ways to treat and prevent this disease.

In hepatocellular carcinoma, dysbiosis along the gut–liver axis increases secondary bile acids and LPS translocation, activating TLR4 on hepatocytes and Kupffer cells to drive fibrosis and tumorigenesis.

In pancreatic ductal adenocarcinoma, distinct intratumoral and gut communities (e.g., Fusobacterium, Pseudomonas) modulate the immune microenvironment through TLR activation, MDSC recruitment, and metabolites such as TMAO and 3‑IAA.

Anti‑tumorigenic functions of the microbiome

Commensal microbes also exert protective effects via:

• Production of SCFAs (butyrate, propionate), which support epithelial barrier integrity, promote regulatory and effector T‑cell balance, and can directly constrain proliferation and NFAT/NF‑κB signaling in tumor cells.(38)

• Induction of anti-tumor immunity through pattern recognition receptor signaling and molecular mimicry, where bacterial epitopes resemble tumor neoantigens, potentially broadening T‑cell repertoires.(39)

Follow these suggestions to help establish a “normal microbiome”:

• Eat a diverse range of foods.

• Eat lots of vegetables, legumes, and beans.

• Eat fermented foods like yogurt (unsweetened), kefir, apple cider vinegar, kombucha, pickles, sauerkraut, tempeh, and kimchi.

• Eat foods rich in polyphenols (dark fruits). Include resveratrol supplements.

• Eat prebiotic fiber. Glucomannan is a dietary fiber (soluble and insoluble) made from the root of the konjac plant.

• Eat chia seeds, high in insoluble and soluble fiber.

• Eat less sugar and sweeteners.

• Reduce stress.

• Avoid taking antibiotics unnecessarily.

• Stop snacking.

• Exercise regularly.

• Spend time outdoors in the natural world to get exposure to millions of microbes, many of which can benefit microbiome diversity.

• Get enough sleep.

The consumption of fermented foods may be particularly important in restoring/maintaining a normal microbiome. Large cohort studies as well as limited interventional studies have linked the consumption of fermented foods with weight maintenance and decreased diabetes, cancer, and cardiovascular disease risks. (40)

Management of cancer cachexia

A high percentage of patients with cancer are nutritionally impaired and at risk for malnutrition.(41) Cancer-associated cachexia is a disorder characterized by loss of body weight with specific losses of skeletal muscle and adipose tissue. (42, 43) It is characterized by a negative protein and energy balance. Cancer cachexia is driven by a variable combination of reduced food intake and metabolic changes, including elevated energy expenditure, excess catabolism, and inflammation. (42) Cancer cachexia is defined as weight loss greater than 5%, or BMI <20 and any degree of weight loss >2%; or skeletal muscle index consistent with sarcopenia (males <7·26 kg/m²; females <5·45 kg/m²). (44) Cancer cachexia is associated with reduced physical function, reduced tolerance to anticancer therapy, and reduced survival. (42, 43) Cancer cachexia is common in patients with advanced cancer.

The therapeutic strategy is to address coexisting treatable factors. The treatment of cancer cachexia should be chosen in a way that can be continued according to the patient’s condition and lifestyle. Patients with advanced cancer who can complete an exercise program show improvements in physical function and quality of life (see exercise] in section on lifestyle interventions for the treatment of cancer). In RCTs in patients with advanced cancer, nutritional therapy alone has not demonstrated consistent efficacy on weight, quality of life, and survival. (45, 46) Nevertheless, we suggest three nutrient-dense meals a day (following the Banting Diet). Intermittent fasting/time-restricted feeding should be avoided (except during chemotherapy); however, patients should avoid snacking between meals and should avoid eating within 3-4 hours before going to sleep (to promote autophagy while sleeping).

Shukla et al demonstrated that ketone body-induced intracellular metabolomic reprogramming in pancreatic cancer cells leads to a significantly diminished cachexia in cell line models. The cachectic phenotype is in part due to metabolic alterations in tumor cells, which can be reverted by a ketogenic diet, causing reduced tumor growth and inhibition of muscle and body weight loss. (47) In addition, we suggest a complete nutritional “shake” containing superfoods such as plant protein, super green, omega-3 fatty acids, vitamins, adaptogenic herbs, probiotics, fiber, mushrooms, and berries (e.g., Ka’Chava ™ https://www.kachava.com/ and 310 Shakes™ https://310nutrition.com/). These “superfood shakes” are preferred over regular protein shakes. Tube feeding should be avoided as this may negatively impact quality of life. Pharmacological therapies for cachexia have limited efficacy and are difficult to improve the severely reduced muscle mass in patients with cachexia. (43) Anamorelin, a ghrelin receptor agonist, is currently the only drug available for the indication of cancer cachexia in a limited number of countries. (48) However, it has been reported that anamorelin elevates IGF-1 which promotes tumor growth. (49)

Studies have shown that 20% of cancer-related deaths were directly due to TLR-induced cancer cachexia, in which cancer cells released heat shock proteins that acted as TLR-4 agonists in macrophages, skeletal muscle, and fat cells, causing downstream signal transduction. EGCG effectively downregulates the TLR-4 signal pathway. (50)

In Conclusion

A carbohydrate-restricted ketogenic diet is recommended for patients with cancer. This approach involves limiting carbohydrate intake to fewer than 25 grams per day and consuming a diet rich in saturated and omega-3 fatty acids. Patients should avoid high-glycemic index foods and all processed foods. (5) Contrary to popular belief, saturated fatty acids are health-supportive, whereas processed omega-6 vegetable oils should be avoided. (51, 52) Intermittent fasting and periodic 2- to 3-day water-only fasts may enhance the effectiveness of standard chemotherapy and radiotherapy.

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