Walnuts: Cancer Research

Table of Contents

1. How to Read Cancer-and-Food Evidence
2. What in a Walnut Researchers Study
3. People: The Breast Cancer Pre-Surgery Trial
4. People: Walnuts, Urolithins and Colon Polyps
5. People: Prostate Markers in Men
6. People: Cohort and Case-Control Studies
7. People: Nut-and-Cancer Meta-Analyses
8. Animal Studies: Mice Fed Walnuts
9. Cell and Test-Tube Studies
10. What Is Not Known
11. Cautions and Context
12. Connections
13. Key Research Papers
14. Featured Videos

How to Read Cancer-and-Food Evidence

Cancer research on any single food sits on a ladder of evidence, and each rung answers a different question.

• Randomised trials with cancer outcomes — people are assigned at random to eat the food or not, and researchers count who develops cancer, has a recurrence, or dies. This is the only design that can show a food prevents or treats cancer. For walnuts alone, no such trial exists.
• Short feeding trials with biomarkers — people eat walnuts for days or weeks and researchers measure something in blood, urine, stool or tumour tissue (a gene-activity pattern, an inflammation marker, PSA). These show that walnuts can change a measurement; they do not show that the change alters anyone's cancer risk or outcome.
• Observational studies — cohorts that follow thousands of people and compare frequent nut eaters with non-eaters, or case-control studies that ask people with and without cancer what they ate. These find associations. People who eat nuts often differ from those who don't in many other ways (smoking, exercise, income, overall diet), and statistical adjustment can only partly correct for that. Association is not causation.
• Animal studies — usually mice given a carcinogen, mice bred to develop tumours, or mice implanted with human cancer cells, then fed a diet with or without walnuts. Results in mice often do not carry over to people.
• Cell and test-tube studies — cancer cells in a dish exposed to walnut extracts or purified walnut compounds. These can suggest mechanisms, but the concentrations, the absence of digestion and the absence of a whole body make them the weakest guide to what happens when a person eats a walnut.

Every result below is labelled with its rung.

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What in a Walnut Researchers Study

Researchers interested in walnuts and cancer usually point to a handful of constituents. A 2023 review from a colon cancer prevention group summarises them: the plant omega-3 fat alpha-linolenic acid (ALA), tocopherols (forms of vitamin E), antioxidant polyphenols including ellagitannins, and prebiotic fibre at about 2 grams per ounce.

• Ellagitannins and urolithins. Ellagitannins are large polyphenol molecules concentrated in the thin papery skin of the kernel; the main one in walnuts is called pedunculagin. In the gut they break down to release ellagic acid, which gut bacteria then convert into smaller, absorbable compounds called urolithins (urolithin A is the best studied). People differ widely in how much urolithin their gut bacteria make — the parallel article on the gut microbiome and urolithins covers this in depth.
• Alpha-linolenic acid. Walnuts are the one common nut with a substantial amount of this plant omega-3 fat (see ALA, omega-3 and the brain). In several of the mouse studies below, walnut feeding raised omega-3 levels in the animals' tissues and tumours.
• Gamma-tocopherol. Walnuts carry vitamin E mostly as gamma-tocopherol rather than the alpha form found in most supplements. One small trial in men (below) showed walnut eating raised blood gamma-tocopherol.
• Phytosterols, carotenoids and melatonin. The Marshall University group that ran the breast cancer studies lists these alongside omega-3 fats and polyphenols as walnut components that may affect cancer growth — a reason for the hypothesis, not evidence of an effect.

The same 2023 review lays out the rationale for studying them in colorectal cancer prevention; it is a review of mechanisms and early studies, not new evidence that walnuts prevent cancer.

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People: The Breast Cancer Pre-Surgery Trial

Evidence type: small randomised feeding trial in people, measuring tumour gene activity (a biomarker, not a cancer outcome).

The most direct human walnut-and-cancer study is a pilot trial published in 2019 by W. Elaine Hardman and colleagues at Marshall University, building on their earlier mouse work. Women with breast lumps large enough for both a research biopsy and a pathology biopsy were randomly assigned to a walnut group or a control group; there was no placebo. Immediately after the biopsy, women in the walnut group began eating 2 ounces (about 56 grams) of walnuts a day until their surgery, roughly two weeks later. All women who stayed in the trial were confirmed to have breast cancer.

At surgery, the researchers took a second tumour sample and compared each woman's gene activity before and after. In the walnut group (5 women) versus the control group (5 women), RNA sequencing found that the expression of 456 genes in the tumour changed significantly with walnut eating. A pathway analysis program classified the changes as activating pathways that promote apoptosis (programmed cell death) and cell adhesion, and inhibiting pathways that promote cell proliferation and migration.

What this does and does not show:

• It shows that two weeks of walnut eating was associated with a measurable shift in tumour gene activity in a direction the authors describe as unfavourable to cancer growth.
• It does not show that any tumour shrank, grew more slowly, or that any woman's outcome changed. Tumour size, recurrence and survival were not the outcomes.
• With 10 women in total, chance findings are a real possibility, and gene-pathway software interprets patterns that have not been confirmed by a clinical result.
• The authors themselves frame the result as supporting a hypothesis: that walnut consumption "could" suppress breast cancer growth in humans. No larger follow-up trial with clinical outcomes has been reported.

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People: Walnuts, Urolithins and Colon Polyps

Evidence type: single-group feeding study in people, measuring urine metabolites, blood markers and polyp tissue (biomarkers).

A research group at the University of Connecticut, which has studied walnuts and colon cancer in mice for years, has reported two human walnut studies, each with 39 participants.

The gut-bacteria report (2024). Participants ate 2 ounces of walnuts a day for 21 days, and the team collected stool and urine before and after. The make-up of participants' gut bacteria differed significantly before and after the three weeks of walnuts. Thirteen bacterial genera became more abundant, including Roseburia, Butyricicoccus, Gordonibacter and Eubacterium eligens. Twenty-six genera were statistically linked to levels of seven urolithin compounds in urine.

The inflammation and polyp-tissue report (2025). This study examined walnut eating, urine urolithins, blood inflammation markers and colon polyp tissue from 39 participants. They showed a widely divergent ability to make urolithins — nine different urolithin metabolites were measured. People who made more urolithin A had lower levels of several inflammation-related blood markers (including soluble ICAM-1, soluble IL-6 receptor, TRAIL and MCP-2), and higher levels of the gut hormone peptide YY. Imaging of the polyp tissue showed altered patterns of cell clusters, including significantly lower levels of two markers, vimentin and CD163, in people who formed more urolithin A.

What this does and does not show:

• It shows that, in people eating walnuts, the ability to produce urolithin A tracks with a less inflamed profile in blood and in polyp tissue.
• Neither report describes a control group that did not eat walnuts; the 2025 analysis compares people with each other according to how they metabolised walnuts. Being a high urolithin producer may itself reflect other differences in the gut or in health.
• No polyp growth, polyp recurrence or cancer outcome was measured. The authors conclude that the link between urolithin A and inflammation is a reason for further study of urolithins in cancer prevention.

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People: Prostate Markers in Men

Evidence type: small randomised crossover trials in people, measuring PSA and vitamin E levels (biomarkers).

PSA (prostate-specific antigen; see PSA Test) is a blood protein that rises with prostate enlargement, inflammation and cancer. Two small trials checked whether walnuts move it.

• A null result (2007). In a 12-month randomised crossover study of 40 middle-aged men, a walnut-supplemented diet (on average 35 grams a day, 12% of energy) for 6 months was compared with 6 months of the usual diet. Mean PSA at the end of the walnut period was 1.05 µg/L versus 1.06 µg/L at the end of the control period — no difference (P = 0.86). The authors concluded that short-term walnut eating is unlikely to affect PSA adversely.
• A small trend (2008). In an 8-week crossover study of 21 older men at risk for prostate cancer, adding 75 grams of walnuts a day (worked into their usual diet without adding calories) did not change total PSA. The ratio of free PSA to total PSA rose, but this only approached statistical significance (P = 0.07). Blood gamma-tocopherol rose (approaching significance, P = 0.08) and the ratio of alpha- to gamma-tocopherol fell significantly (P = 0.01). The authors read this as walnuts possibly improving prostate biomarkers; with one non-significant trend in a 21-man study, the finding is tentative.

Neither trial measured prostate cancer itself. Taken together, they show that walnuts did not raise or lower PSA in these men.

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People: Cohort and Case-Control Studies

Evidence type: observational studies in people — associations, which cannot prove that nuts caused any difference.

Colon cancer survival: CALGB 89803 (2018)

This is the study most often quoted on nuts and cancer survival. It followed 826 patients with stage III colon cancer (cancer that has reached nearby lymph nodes) who were taking part in a chemotherapy trial and filled in food questionnaires. After a median 6.5 years, patients who reported eating two or more servings of nuts a week, compared with those who ate none, had an adjusted hazard ratio (HR) of 0.58 for disease-free survival (95% confidence interval 0.37–0.92) and 0.43 for overall survival (0.25–0.74). An HR of 0.43 means the rate of death in the nut-eating group was 57% lower over the follow-up period after statistical adjustment. In a subgroup analysis, the association was confined to tree nuts (disease-free survival HR 0.54; overall survival HR 0.47); peanuts did not show it. Walnuts were counted among the tree nuts but were not analysed separately in the abstract.

The authors' own conclusion is careful: diets with more nuts "may be associated" with less recurrence and death. Nut intake was self-reported, nobody was assigned to eat nuts, and people who eat nuts regularly may differ in other ways that matter for survival.

PREDIMED: walnut eating and cancer deaths (2013)

PREDIMED was a Spanish trial in 7,216 men and women aged 55 to 80 at high cardiovascular risk (covered in Heart Health and PREDIMED). Its researchers also analysed participants' reported nut eating at the start of the study as an observational exposure. Over a median 4.8 years there were 130 cancer deaths. People eating nuts more than 3 servings a week had 39% lower total mortality than non-eaters (HR 0.61), and the abstract reports a similar association with cancer deaths.

The full text breaks walnuts out separately. In its fully adjusted model, people eating walnuts more than 3 servings a week (1 serving = 28 g) had an HR for cancer death of 0.46 (95% CI 0.27–0.79) compared with people who rarely or never ate them; for nuts other than walnuts the HR was 0.75 (0.44–1.27), which was not statistically significant (full text, Table 4). This rests on only 20 cancer deaths in the high-walnut group. The authors suggest the higher polyphenol content of walnuts as one possible explanation; that is a hypothesis.

PREDIMED: breast cancer as a trial outcome (2015)

Breast cancer was a prespecified secondary outcome of PREDIMED for 4,152 women aged 60 to 80. Over a median 4.8 years, 35 cases were confirmed. Compared with the control group (advised to cut fat), the hazard ratio was 0.32 (95% CI 0.13–0.79) in the Mediterranean diet plus extra-virgin olive oil group and 0.59 (0.26–1.35) in the Mediterranean diet plus mixed nuts group. The nut group's result was not statistically significant: the confidence interval includes no effect. The nut supplement was mixed nuts, half of them walnuts (the breakdown is in the PREDIMED article), so this is not a walnut-only test, and the authors note the results come from few cases. PREDIMED's main 2013 report was retracted and republished in 2018 after departures from the randomisation protocol were found for some participants; the republished analysis, which reports results similar after omitting those 1,588 participants, is listed below.

Three large US cohorts: no association (2021)

The biggest observational study on the question pooled the Nurses' Health Study, the Nurses' Health Study II and the Health Professionals Follow-up Study: 180,832 women and 45,560 men followed for nearly 5.9 million person-years, with 44,561 cancers. Nut intake (including walnuts as a separate category) was re-measured every 2–4 years. Compared with non-consumers, eating nuts 5 or more times a week was not associated with total cancer (HR 0.99, 95% CI 0.94–1.04), lung, colorectal (HR 1.07), bladder, breast (HR 0.96) or aggressive prostate cancer (HR 1.18, 0.92–1.51). The authors concluded that frequent nut consumption was not associated with the risk of total cancer or these common cancers. This null finding, from the largest data set, is an important counterweight to the smaller positive studies.

A case-control study of breast cancer (2015)

A Mexican study compared 97 women with breast cancer and 104 women without it, asking about lifelong consumption of peanuts, walnuts and almonds. High consumption was linked to a 2- to 3-fold lower risk; low or moderate consumption showed no association. Case-control studies rely on people remembering a lifetime of diet after a diagnosis, which is prone to recall bias, and this one was small. It sits on a low rung of the ladder.

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People: Nut-and-Cancer Meta-Analyses

Evidence type: pooled observational studies in people. These combine associations; they do not convert them into proof of cause.

None of these meta-analyses could isolate walnuts reliably; they pool total nuts, tree nuts and peanuts.

• Wu and colleagues, 2015 (36 observational studies): highest versus lowest nut intake was associated with lower overall cancer incidence (RR 0.85, 95% CI 0.76–0.95), colorectal cancer (RR 0.76; 3 studies), endometrial cancer (RR 0.58; 2 studies) and pancreatic cancer (RR 0.68; 1 study). No significant association was found for other cancers. The authors note the scarcity of data for individual cancers.
• Aune and colleagues, 2016 (20 prospective studies): each 28 grams a day more of nuts was associated with a 15% lower risk of total cancer (RR 0.85, 0.76–0.94; 8 studies). Results were similar for tree nuts and peanuts.
• Chen and colleagues, 2017 (18 prospective studies): high versus low nut intake was associated with 13% lower cancer mortality (RR 0.87, 0.80–0.93; 11 studies, 21,353 deaths), and dose-response analyses suggested mortality risk levelled off at about 3 servings a week (12 grams a day).
• Long and colleagues, 2020 (33 prospective studies, more than 50,000 cancer cases): high nut intake was associated with lower overall cancer risk (RR 0.90, 0.85–0.95), especially digestive-system cancers (RR 0.83). Among nut types, only tree nuts showed a significant association.
• Naghshi and colleagues, 2021 (43 articles on cancer risk, 9 on cancer mortality): highest versus lowest total nut intake was associated with lower cancer risk (pooled effect 0.86, 0.81–0.92); tree nuts 0.87 (0.78–0.96). Each 5 grams a day more of total nuts was associated with 3% lower overall cancer risk and 25% lower colon cancer risk in the dose-response analysis.
• Balali and colleagues, 2023 — prostate cancer, a null result (11 articles, 287,786 participants, 32,213 prostate cancers): no significant association between nut intake and total (RR 0.94, 0.85–1.04), advanced (RR 1.10, 0.98–1.24), non-advanced or fatal prostate cancer, and no dose-response relationship. There were not enough data on walnuts specifically to analyse them.

The pattern across these pooled analyses is a modest inverse association between nut eating and some cancers — most consistently digestive-system cancers — alongside clear null results for prostate cancer and, in the large 2021 US cohort analysis, for total cancer. Associations of 10–15% are the size that unmeasured differences between nut eaters and non-eaters could plausibly produce.

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Animal Studies: Mice Fed Walnuts

Evidence type: animal studies. Every result in this section was found in mice, not people.

Breast cancer in mice

• Implanted human breast cancer, 2008. In nude mice (mice without a working immune system, so human tumours can grow in them) implanted with MDA-MB 231 human breast cancer cells, switching the diet to include ground walnuts — an amount the authors scaled to 56 grams a day in a person — was followed by a tumour growth rate of 2.9 mm³/day versus 14.6 mm³/day in mice not given walnuts. In these mice, tumour cell proliferation fell but cell death did not change, and omega-3 fats (EPA and DHA) rose in the liver. The authors called it a pilot study.
• Mice bred to develop breast tumours, 2011. In a strain of mice genetically programmed to develop mammary tumours, a walnut-containing diet from weaning significantly reduced the share of mice developing a tumour, the number of tumours per mouse and tumour size. In these mice, the omega-3 content alone did not account for the full effect when compared with another diet.

Prostate cancer in mice

• Implanted human prostate cancer, 2013. In nude mice injected with LNCaP human prostate cancer cells, 3 of 16 walnut-fed mice (18.7%) developed tumours versus 14 of 32 mice (44%) on the control diet, and in the walnut-fed mice the final average tumour size was about one quarter of the controls'.
• Mice bred to develop prostate tumours, 2014. In TRAMP mice fed for 18 weeks, diets whose fat came from whole walnuts or walnut oil reduced prostate tumour size, plasma IGF-1 (a growth-promoting hormone) and cholesterol compared with a diet of other oils blended to match walnut's fatty-acid profile. Because the walnut-matched oil blend did not have the effect, the authors concluded the effect in these mice was not due to walnut's omega-3 fats but to some other component of the walnut's fat.

Colon cancer in mice

• Carcinogen-induced colon tumours, 2016. In mice given the colon carcinogen azoxymethane, a standard diet containing 9.4% walnuts gave a modest 1.3-fold reduction in tumour numbers, and a Western-style diet with 7% walnuts gave a significant 2.3-fold reduction in male mice. Higher walnut levels lacked this effect, particularly in female mice — the authors suggest there may be an optimal amount. Walnut feeding also shifted the mice's gut bacteria.
• Implanted human colon cancer, 2015. In mice implanted with HT-29 human colon cancer cells and fed walnuts for 25 days, omega-3 fats rose and arachidonic acid fell in the tumours, final tumour size was negatively correlated with tumour omega-3 content, and several microRNAs (small molecules that regulate genes) changed in tumour tissue.
• Obesity and intestinal tumours, 2018. In mice genetically prone to intestinal tumours and fed a high-fat diet, adding 7.6% walnuts reduced tumour number in one male strain (3.7 to 2.5 tumours per mouse) and limited tumour growth in another male strain. In normal mice, walnuts did not change body metabolism.
• Walnut extract and colitis-associated cancer, 2019. A concentrated walnut phenolic extract, given by stomach tube rather than as food, reduced colitis severity and tumour development in mouse models of inflamed-bowel-associated colon cancer. This tested an extract, not whole walnuts.

Mouse findings are a reason to run human trials, not a substitute for them. The mice were given carcinogens, engineered to develop tumours, or implanted with human cancer cells in a body with no immune system; the walnut doses were scaled from body weight; and many promising mouse results across nutrition research have not been repeated in people.

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Cell and Test-Tube Studies

Evidence type: laboratory studies in cancer cells grown in dishes. Every result in this section was found in cells, not in people or animals.

• Urolithins in prostate cancer cells (2014). In LNCaP prostate cancer cells, urolithins A and B — the gut-bacterial products of walnut ellagitannins — lowered the production of PSA and of the androgen receptor (the protein that lets male hormones drive prostate cells), reduced the receptor's binding to DNA, and induced cell death, which in these cells went with lower levels of the survival protein Bcl-2.
• Walnut extract and colon cancer stem cells (2016). In cell culture, a walnut phenolic extract inhibited survival and self-renewal of a stem-cell-like subset of HCT116 colon cancer cells and lowered stem-cell markers; the whole extract worked more strongly in these cells than its individual compounds (catechin, chlorogenic acid, ellagic acid, gallic acid) tested alone. It also lowered stem-cell markers in colon cancer cells taken from a patient's tumour and grown in the lab.
• Walnut extract and inflammatory signalling (2019). In COLO205 colon cells in culture, the same type of walnut phenolic extract reduced the inflammatory messengers IL-8 and IL-1α and blocked activation of NF-κB, a master switch for inflammation.

Cell studies expose cells directly to compounds at chosen concentrations, without digestion, absorption, the liver, or the gut bacteria that make urolithins in the first place. Whether the concentrations reached in a person's bloodstream or prostate after eating walnuts are anywhere near those used in the dish is generally not known.

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What Is Not Known

Plainly: no clinical trial has shown that eating walnuts prevents cancer or treats cancer in people. The state of the evidence:

• No walnut trial has a cancer outcome. The human walnut trials measured tumour gene activity (10 women, 2 weeks), urine and blood markers (39 people, 3 weeks) or PSA (40 and 21 men). None counted cancers, recurrences or deaths.
• The one randomised trial that did count cancers used mixed nuts within a whole diet, and the nut arm's breast cancer result was not statistically significant.
• The observational signals point in different directions. Colon cancer survivors who ate tree nuts did better in CALGB 89803, and frequent walnut eaters in PREDIMED had fewer cancer deaths; the largest pooled US cohort analysis found no association between nut eating and total cancer, and prostate cancer meta-analysis found none either.
• Walnut-specific data are thin. Most large studies pool all nuts. The prostate meta-analysis could not analyse walnuts at all for lack of data.
• It is not known whether the gut-bacteria differences matter. People vary greatly in how much urolithin they make; whether that changes any cancer outcome is untested.
• It is not known whether walnuts interact with cancer treatment. None of the studies above tested walnuts alongside chemotherapy, hormone therapy or radiotherapy for safety or effect.

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Cautions and Context

• Tree nut allergy. Walnuts are a tree-nut allergen; for people with that allergy, the research above does not apply.
• Amounts. The human studies gave 2 ounces (about 56 g) a day for 2–3 weeks, 35 g a day for 6 months, or 75 g a day for 8 weeks. These are amounts used in trials, not established doses for any outcome.
• Not a replacement for treatment. Nothing in this research tests walnuts as an alternative to screening or cancer treatment. Decisions about diet during cancer treatment belong with the treating oncology team.
• Funding. Some walnut papers disclose ties to a walnut-industry body; the 2013 PREDIMED nut-mortality paper, for example, lists one author as having received grants from such a body and sitting on its scientific advisory committee. Industry funding does not make a result wrong, but it is part of the context readers may want to know.
• Whole walnuts, not extracts. Several animal and cell results used concentrated walnut extracts or isolated urolithins, which are not the same thing as eating walnuts.

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Connections

• Walnuts — the main topic page
• Walnuts — Benefits Deep Dive — the hub for the walnut articles
• Walnuts: Gut Microbiome and Urolithins — the parallel article on ellagitannin metabolism
• Walnuts: Heart Health and PREDIMED — the trial behind two of the studies here
• Walnuts: ALA, Omega-3 and the Brain — the plant omega-3 in detail
• Walnuts: Nutrient Profile — the composition table
• Nuts — all nut pages
• Ellagic Acid — the polyphenol released from walnut ellagitannins
• Breast Cancer
• Prostate Cancer
• Colorectal Cancer
• PSA Test — the marker measured in the prostate trials
• Vitamin E — including gamma-tocopherol
• Pomegranate: Prostate and PSA — the other big urolithin food
• Flaxseed: Lignans and Hormone-Related Cancers — a comparable seed evidence base
• Oncology — the cancer section

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Key Research Papers

1. Hardman WE, Primerano DA, Legenza MT, Morgan J, Fan J, Denvir J. Dietary walnut altered gene expressions related to tumor growth, survival, and metastasis in breast cancer patients: a pilot clinical trial. Nutrition Research. 2019;66:82-94. PubMed PMID: 30979659
2. Moussa MR, Fan N, Birk J, Provatas AA, Mehta P, Hatano Y, et al. Systemic Inflammation and the Inflammatory Context of the Colonic Microenvironment Are Improved by Urolithin A. Cancer Prevention Research. 2025;18(4):235-250. PubMed PMID: 39995164
3. Liu H, Birk JW, Provatas AA, Vaziri H, Fan N, Rosenberg DW, et al. Correlation between intestinal microbiota and urolithin metabolism in a human walnut dietary intervention. BMC Microbiology. 2024;24(1):476. PubMed PMID: 39548408
4. Simon JA, Tanzman JS, Sabaté J. Lack of effect of walnuts on serum levels of prostate specific antigen: a brief report. Journal of the American College of Nutrition. 2007;26(4):317-20. PubMed PMID: 17906182
5. Spaccarotella KJ, Kris-Etherton PM, Stone WL, Bagshaw DM, Fishell VK, West SG, et al. The effect of walnut intake on factors related to prostate and vascular health in older men. Nutrition Journal. 2008;7:13. PubMed PMID: 18454862
6. Fadelu T, Zhang S, Niedzwiecki D, Ye X, Saltz LB, Mayer RJ, et al. Nut Consumption and Survival in Patients With Stage III Colon Cancer: Results From CALGB 89803 (Alliance). Journal of Clinical Oncology. 2018;36(11):1112-1120. PubMed PMID: 29489429
7. Guasch-Ferré M, Bulló M, Martínez-González MÁ, Ros E, Corella D, Estruch R, et al. Frequency of nut consumption and mortality risk in the PREDIMED nutrition intervention trial. BMC Medicine. 2013;11:164. PubMed PMID: 23866098
8. Toledo E, Salas-Salvadó J, Donat-Vargas C, Buil-Cosiales P, Estruch R, Ros E, et al. Mediterranean Diet and Invasive Breast Cancer Risk Among Women at High Cardiovascular Risk in the PREDIMED Trial: A Randomized Clinical Trial. JAMA Internal Medicine. 2015;175(11):1752-1760. PubMed PMID: 26365989
9. Estruch R, Ros E, Salas-Salvadó J, et al. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet Supplemented with Extra-Virgin Olive Oil or Nuts. The New England Journal of Medicine. 2018;378(25):e34. PubMed PMID: 29897866
10. Fang Z, Wu Y, Li Y, Zhang X, Willett WC, Eliassen AH, et al. Association of nut consumption with risk of total cancer and 5 specific cancers: evidence from 3 large prospective cohort studies. The American Journal of Clinical Nutrition. 2021;114(6):1925-1935. PubMed PMID: 34582546
11. Soriano-Hernandez AD, Madrigal-Perez DG, Galvan-Salazar HR, Arreola-Cruz A, Briseño-Gomez L, Guzmán-Esquivel J, et al. The protective effect of peanut, walnut, and almond consumption on the development of breast cancer. Gynecologic and Obstetric Investigation. 2015;80(2):89-92. PubMed PMID: 26183374
12. Wu L, Wang Z, Zhu J, Murad AL, Prokop LJ, Murad MH. Nut consumption and risk of cancer and type 2 diabetes: a systematic review and meta-analysis. Nutrition Reviews. 2015;73(7):409-25. PubMed PMID: 26081452
13. Aune D, Keum N, Giovannucci E, Fadnes LT, Boffetta P, Greenwood DC, et al. Nut consumption and risk of cardiovascular disease, total cancer, all-cause and cause-specific mortality: a systematic review and dose-response meta-analysis of prospective studies. BMC Medicine. 2016;14(1):207. PubMed PMID: 27916000
14. Chen GC, Zhang R, Martínez-González MA, Zhang ZL, Bonaccio M, van Dam RM, et al. Nut consumption in relation to all-cause and cause-specific mortality: a meta-analysis 18 prospective studies. Food & Function. 2017;8(11):3893-3905. PubMed PMID: 28875220
15. Long J, Ji Z, Yuan P, Long T, Liu K, Li J, et al. Nut Consumption and Risk of Cancer: A Meta-analysis of Prospective Studies. Cancer Epidemiology, Biomarkers & Prevention. 2020;29(3):565-573. PubMed PMID: 32041895
16. Naghshi S, Sadeghian M, Nasiri M, Mobarak S, Asadi M, Sadeghi O. Association of Total Nut, Tree Nut, Peanut, and Peanut Butter Consumption with Cancer Incidence and Mortality: A Comprehensive Systematic Review and Dose-Response Meta-Analysis of Observational Studies. Advances in Nutrition. 2021;12(3):793-808. PubMed PMID: 33307550
17. Balali A, Askari G, Anjom-Shoae J, Sadeghi O. Association between nut consumption and prostate cancer risk in adults: A systematic review and dose-response meta-analysis of observational studies. Nutrition, Metabolism, and Cardiovascular Diseases. 2023;33(7):1293-1307. PubMed PMID: 37160404
18. Hardman WE, Ion G. Suppression of implanted MDA-MB 231 human breast cancer growth in nude mice by dietary walnut. Nutrition and Cancer. 2008;60(5):666-74. PubMed PMID: 18791931
19. Hardman WE, Ion G, Akinsete JA, Witte TR. Dietary walnut suppressed mammary gland tumorigenesis in the C(3)1 TAg mouse. Nutrition and Cancer. 2011;63(6):960-70. PubMed PMID: 21774594
20. Reiter RJ, Tan DX, Manchester LC, Korkmaz A, Fuentes-Broto L, Hardman WE, et al. A walnut-enriched diet reduces the growth of LNCaP human prostate cancer xenografts in nude mice. Cancer Investigation. 2013;31(6):365-73. PubMed PMID: 23758186
21. Kim H, Yokoyama W, Davis PA. TRAMP prostate tumor growth is slowed by walnut diets through altered IGF-1 levels, energy pathways, and cholesterol metabolism. Journal of Medicinal Food. 2014;17(12):1281-6. PubMed PMID: 25354213
22. Nakanishi M, Chen Y, Qendro V, Miyamoto S, Weinstock E, Weinstock GM, et al. Effects of Walnut Consumption on Colon Carcinogenesis and Microbial Community Structure. Cancer Prevention Research. 2016;9(8):692-703. PubMed PMID: 27215566
23. Tsoukas MA, Ko BJ, Witte TR, Dincer F, Hardman WE, Mantzoros CS. Dietary walnut suppression of colorectal cancer in mice: Mediation by miRNA patterns and fatty acid incorporation. The Journal of Nutritional Biochemistry. 2015;26(7):776-83. PubMed PMID: 25882694
24. Guan F, Tabrizian T, Novaj A, Nakanishi M, Rosenberg DW, Huffman DM. Dietary Walnuts Protect Against Obesity-Driven Intestinal Stem Cell Decline and Tumorigenesis. Frontiers in Nutrition. 2018;5:37. PubMed PMID: 29904634
25. Koh SJ, Choi YI, Kim Y, Kim YS, Choi SW, Kim JW, et al. Walnut phenolic extract inhibits nuclear factor kappaB signaling in intestinal epithelial cells, and ameliorates experimental colitis and colitis-associated colon cancer in mice. European Journal of Nutrition. 2019;58(4):1603-1613. PubMed PMID: 29744610
26. Sánchez-González C, Ciudad CJ, Noé V, Izquierdo-Pulido M. Walnut polyphenol metabolites, urolithins A and B, inhibit the expression of the prostate-specific antigen and the androgen receptor in prostate cancer cells. Food & Function. 2014;5(11):2922-30. PubMed PMID: 25214070
27. Lee J, Kim YS, Lee J, Heo SC, Lee KL, Choi SW, et al. Walnut Phenolic Extract and Its Bioactive Compounds Suppress Colon Cancer Cell Growth by Regulating Colon Cancer Stemness. Nutrients. 2016;8(7):439. PubMed PMID: 27455311
28. Fan N, Fusco JL, Rosenberg DW. Antioxidant and Anti-Inflammatory Properties of Walnut Constituents: Focus on Personalized Cancer Prevention and the Microbiome. Antioxidants (Basel). 2023;12(5):982. PubMed PMID: 37237848

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