Walnuts for Heart Health: The PREDIMED Trial

PREDIMED — Prevencion con Dieta Mediterranea — remains one of the most consequential nutrition trials of the modern era. 7,447 Spanish adults aged 55-80 at high cardiovascular risk were randomized to a Mediterranean diet supplemented with 30 grams of mixed nuts per day (half walnuts), a Mediterranean diet supplemented with extra-virgin olive oil, or a low-fat control diet. After a median 4.8 years, both Mediterranean interventions cut the composite of myocardial infarction, stroke and cardiovascular death by roughly 30% against the reduced-fat control — a corrected hazard ratio of 0.72 for the nuts arm and 0.69 for the olive-oil arm. The trial was retracted and re-published in 2018 after randomization irregularities were found at some sites, and the corrected analysis preserved the finding. PREDIMED is the strongest randomized evidence we have for the Mediterranean pattern, and it is narrower than its reputation: the composite was driven by stroke, and neither cardiovascular death nor all-cause death was significantly reduced. It is also worth knowing that the walnut-specific contribution cannot be separated out — the nuts were a 50/25/25 mix of walnuts, almonds and hazelnuts.

Table of Contents

  1. PREDIMED Trial Background and Design
  2. PREDIMED Primary Cardiovascular Outcomes
  3. What PREDIMED Did Not Show
  4. The 2018 Retraction and Re-Publication
  5. The Nuts Arm vs the Olive Oil Arm
  6. Mechanism: LDL Cholesterol and Lipid Profile
  7. Mechanism: Endothelial Function and Flow-Mediated Dilation
  8. Mechanism: Inflammation, CRP, and Oxidative Stress
  9. Mechanism: Blood Pressure and Vascular Stiffness
  10. Mechanism: Atrial Fibrillation and Arrhythmia
  11. PREDIMED-Plus and the Weight-Loss Extension
  12. Practical Recommendations
  13. Cautions
  14. Key Research Papers
  15. Connections
  16. Featured Videos

PREDIMED Trial Background and Design

PREDIMED was launched in 2003 by Ramon Estruch, Emilio Ros, Jordi Salas-Salvado, and Miguel Martinez-Gonzalez, with funding from the Spanish government and the EU. The trial was designed to test whether a Mediterranean diet could reduce hard cardiovascular endpoints in high-risk primary-prevention patients — not surrogate markers like LDL cholesterol, but actual myocardial infarction, stroke, and cardiovascular death.

This was a meaningful design choice. Most prior dietary intervention trials had been either too small or too short to detect cardiovascular events, or had used surrogate endpoints that did not always translate to clinical outcomes. PREDIMED committed to enrolling enough high-risk participants for long enough to see real events.

Inclusion criteria:

7,447 participants were enrolled across 11 Spanish recruitment sites and randomized to one of three arms:

  1. Mediterranean diet plus mixed nuts (n=2,454) — participants received 30 g/day of mixed nuts free of charge, composed of 15 g walnuts, 7.5 g almonds, and 7.5 g hazelnuts
  2. Mediterranean diet plus extra-virgin olive oil (n=2,543) — participants received 1 liter per week of high-quality EVOO free of charge
  3. Low-fat control diet (n=2,450) — participants received dietary advice to reduce total dietary fat (aim for <30% of calories from fat), with periodic free gifts of non-food items rather than food

All participants received quarterly individual and group dietary counseling sessions throughout the trial. The intervention was sustained for a median of 4.8 years before the trial was stopped early by the Data Safety Monitoring Board for benefit in the Mediterranean arms.

Back to Table of Contents

PREDIMED Primary Cardiovascular Outcomes

The pre-specified primary endpoint was a composite of myocardial infarction, stroke, and cardiovascular death. The trial was stopped early at median 4.8 years because the Data Safety Monitoring Board determined the Mediterranean arms had reached the pre-specified efficacy threshold.

Headline results from the original 2013 NEJM publication (Estruch et al.):

The absolute risk reduction was approximately 1.6 events per 1,000 person-years — meaning that for every roughly 600 high-risk adults adhering to the Mediterranean intervention for one year, one major cardiovascular event was prevented. Over the trial's median 4.8 years, the number needed to treat was about 125 to prevent one composite endpoint.

The benefit was particularly strong for stroke. Pooling both Mediterranean arms, the Cochrane review of Mediterranean-style diets put the stroke reduction at a hazard ratio of 0.60 (95% CI 0.45-0.80) — a fall from roughly 24 strokes per 1,000 people to 14 per 1,000.

Cardiovascular death is a different story, and it matters. The composite endpoint fell, but the trial was powered for the composite, not for its individual parts. In that same Cochrane analysis, PREDIMED showed little or no effect on death from cardiovascular causes (hazard ratio 0.81, 95% CI 0.50-1.32) and no effect at all on death from any cause (hazard ratio 1.00, 95% CI 0.81-1.24). Read plainly: PREDIMED showed that people on the Mediterranean arms had fewer strokes, not that they lived longer.

The trial enrolled high-risk primary-prevention patients, so the absolute event rate was meaningful. In healthy younger populations with lower baseline cardiovascular risk, the relative risk reduction would presumably be similar but the absolute benefit smaller.

Back to Table of Contents

What PREDIMED Did Not Show

PREDIMED is genuinely good evidence, and it is also routinely oversold — including by people selling nuts. Four limits are worth holding on to whenever you see the trial quoted.

  1. It did not show that anyone lived longer. All-cause mortality came out at a hazard ratio of 1.00 (95% CI 0.81-1.24) — completely flat. Cardiovascular mortality did not reach significance either.
  2. The composite was driven by stroke. The trial was designed and powered for the three-part composite, so it was never expected to prove each component on its own. But that also means "walnuts prevent heart attacks" is a stronger claim than PREDIMED supports; "fewer strokes" is the claim the data carry.
  3. Cochrane graded PREDIMED’s mortality evidence as low quality and its stroke evidence as moderate quality, largely because of the randomization problems described in the next section. In that grading system, "low quality" means further research is very likely to change the estimate.
  4. The comparator was reduced-fat advice, not usual diet. The control group was counselled to cut total fat and received non-food gifts rather than free food. Part of the measured gap is the Mediterranean arms doing well; part of it may be the control arm doing worse than it would have on no advice at all.

None of this makes walnuts a bad idea. It means the honest version of the claim is narrower than the headline: in older adults already at high cardiovascular risk, a Mediterranean pattern that includes a daily serving of nuts reduced strokes over about five years, with no demonstrated effect on how long people lived.

Back to Table of Contents

The 2018 Retraction and Re-Publication

In 2018, the New England Journal of Medicine formally retracted the original 2013 PREDIMED paper after methodological concerns were raised by John Carlisle, an anesthesiologist who specializes in detecting statistical irregularities in clinical trial baseline characteristics. Carlisle's analysis suggested that baseline characteristics in PREDIMED were too similar across arms to have arisen from purely individual randomization — raising the possibility that some recruitment sites had used cluster randomization (entire couples, families, or clinic days assigned to the same arm) rather than strict individual randomization.

The PREDIMED investigators acknowledged the concern and re-analyzed the data accounting for the randomization deviations. A subset of approximately 1,588 participants (21% of the trial) had been enrolled with non-individual randomization — primarily through one recruiting site where a single physician had randomized all patients on the same clinic day to the same arm, and a small number of couples who were randomized together.

The re-analysis used appropriate statistical methods to account for the clustering, including sensitivity analyses excluding the affected sites entirely, multivariable models adjusting for cluster effects, and intention-to-treat analysis preserving the as-randomized structure. The corrected analyses preserved the core findings: the Mediterranean intervention arms produced approximately 30% reduction in the primary cardiovascular composite endpoint compared to control. The effect sizes were slightly attenuated in some sensitivity analyses but remained both statistically significant and clinically meaningful.

The trial was re-published in NEJM in 2018 with the corrected analyses (Estruch et al., NEJM 2018). The retraction-and-republication was unusual and uncomfortable, but the scientific community has generally accepted that the PREDIMED finding is real — the methodological issue did not nullify the underlying cardiovascular benefit, just required more careful statistical treatment to demonstrate it. This is what science self-correction looks like in practice.

For interpreting PREDIMED today, the 2018 re-published version is the authoritative reference. Its corrected intention-to-treat estimates, adjusting for baseline characteristics and propensity scores, were a hazard ratio of 0.69 (95% CI 0.53-0.91) for the olive-oil arm and 0.72 (95% CI 0.54-0.95) for the nuts arm, against 288 primary events in total — 96 in the olive-oil group, 83 in the nuts group, and 109 in the control group. Results were similar after omitting all 1,588 participants whose group assignment was known or suspected to have departed from the protocol. Those are the numbers to quote.

Back to Table of Contents

The Nuts Arm vs the Olive Oil Arm

The two Mediterranean arms produced broadly similar overall cardiovascular benefit, but with some differences in specific endpoints. The nuts arm showed:

The EVOO arm showed:

A caution about this kind of comparison: PREDIMED was not designed to test the nuts arm against the olive-oil arm. Each was compared with the control group, and the confidence intervals around the two overlap heavily. Differences between the arms on any single endpoint may be real, or may be what you get when you slice a trial finely enough. Treat arm-versus-arm bullet points — anywhere you see them, including here — as hypothesis, not result.

The two arms are best understood as complementary rather than competing. The traditional Mediterranean diet that PREDIMED was modeling includes both nuts and olive oil, not one or the other. The trial design separated them to test the independent contribution of each, but the practical recommendation for clinical use is to include both.

The walnut-specific contribution within the nuts arm cannot be disentangled at all — the mixed nuts were 50% walnuts, 25% almonds, 25% hazelnuts, and no PREDIMED analysis separates them. Walnut-only trials exist and show benefit on lipids and endothelial function, but they measure surrogate markers over weeks to months, not strokes over years. Sabaté’s pooled analysis of 25 nut trials found, explicitly, that different types of nuts had similar effects on blood lipids. So the claim that walnuts are the most cardiovascular-active of the three is a plausible guess based on their ALA and polyphenol content — not something PREDIMED or any other trial has demonstrated.

Back to Table of Contents

Mechanism: LDL Cholesterol and Lipid Profile

Walnuts produce a consistent, dose-related reduction in LDL cholesterol in controlled feeding trials. Two separate pooled analyses are usually quoted for this, and they are often mixed up with each other, so it is worth keeping them apart.

Banel and Hu (2009) pooled 13 walnut-specific trials totalling 365 participants, with diets lasting 4 to 24 weeks:

Two caveats the headline numbers hide. First, walnuts supplied 10 to 24% of total calories in those trials — for a 2,000-calorie diet that is roughly 30 to 70 g of walnuts a day, so the upper end of the tested range is well above a single 30 g serving. Second, the authors' own conclusion was cautious: "Larger and longer-term trials are needed to address the effects of walnut consumption on cardiovascular risk and body weight." That was 2009, and it is still largely true.

Sabaté, Oda and Ros (2010) pooled 25 trials of nuts in general (not walnuts specifically) at a mean intake of 67 g/day:

So the honest summary is: walnuts lower LDL and total cholesterol by around 9 to 11 mg/dL at doses at or above a generous serving; they do not raise HDL; and they lower triglycerides only if yours are already high.

The mechanism involves several overlapping effects:

  1. Replacement of saturated fat with polyunsaturated fat. When walnut PUFA replaces dietary saturated fat (butter, cheese, fatty meat), the standard lipid-improvement mechanism kicks in: PUFA suppresses hepatic SREBP-2 less than saturated fat, leading to reduced HMG-CoA reductase activity and reduced cholesterol synthesis.
  2. Bile acid binding by walnut fiber. Walnut fiber (about 2 g per ounce) binds bile acids in the small intestine and increases fecal bile acid excretion. The liver replaces lost bile acids by upregulating cholesterol-to-bile acid conversion via CYP7A1, pulling cholesterol out of LDL particles in circulation.
  3. Phytosterol content. Walnuts contain approximately 30 mg of phytosterols per ounce. Phytosterols compete with cholesterol for absorption in the small intestine, reducing cholesterol uptake. The effect is modest at walnut doses but contributes.
  4. ALA reduction of hepatic VLDL secretion. ALA-derived metabolites suppress hepatic apoB100 secretion modestly, reducing VLDL particle assembly and downstream LDL production.

What that means clinically: a 9 to 10 mg/dL LDL reduction is real but modest — roughly a 7% drop, against the 30 to 50% a moderate- or high-intensity statin delivers. Comparing walnuts to "a low-intensity statin dose" flatters the walnuts. If you have mild hyperlipidemia and want to try diet first, daily walnuts are a sensible part of that attempt. If you have high cardiovascular risk and a statin is indicated, walnuts sit alongside the drug; they are nowhere near a substitute for it.

Back to Table of Contents

Mechanism: Endothelial Function and Flow-Mediated Dilation

Endothelial dysfunction — impaired ability of the vascular endothelium to produce nitric oxide and dilate in response to shear stress — is one of the earliest detectable abnormalities in atherosclerosis, preceding plaque formation by years. Brachial artery flow-mediated dilation (FMD) measured by ultrasound is the standard non-invasive test of endothelial function.

Walnut intervention does improve FMD, though by less than is often claimed. The 2024 systematic review and meta-analysis by Hsu and colleagues pooled six walnut trials in 250 participants and found a mean FMD improvement of 0.94 percentage points (95% CI 0.12 to 1.75, P = 0.02) — statistically significant, but with a confidence interval whose lower bound is close to nothing. A broader meta-analysis of nuts generally (Neale and colleagues, 32 randomized trials) found a similar 0.79-point improvement (95% CI 0.35 to 1.23). Both reviews call for more and better trials.

The same 2024 review found no significant effect of walnuts on the endothelial adhesion molecules ICAM-1 or VCAM-1. So the FMD signal is not accompanied by a matching change in the adhesion-molecule markers you would expect to move alongside it — a reason to treat FMD here as a promising surrogate rather than settled proof of vascular benefit.

The mechanism involves at least three overlapping pathways:

  1. L-arginine availability. Walnuts contain approximately 0.6 g of L-arginine per ounce. L-arginine is the substrate for endothelial nitric oxide synthase (eNOS), and increased substrate availability supports increased NO production.
  2. ALA-mediated reduction of inflammation around the endothelium. Reduced inflammatory cytokine production reduces inducible nitric oxide synthase (iNOS)-driven inflammation that depletes the tetrahydrobiopterin (BH4) cofactor needed by eNOS, indirectly restoring eNOS function.
  3. Polyphenol effects on eNOS expression. Walnut polyphenols, particularly urolithins, increase eNOS expression in endothelial cells and reduce reactive oxygen species production that would otherwise scavenge NO.

There is an acute effect too, but it is narrower than it is usually described. Cortés and colleagues (2006) fed 12 healthy volunteers and 12 people with high cholesterol two high-fat test meals a week apart — one with 40 g of walnuts added, one with 25 g of olive oil — and measured brachial FMD four hours later. FMD was better after the walnut meal than after the olive-oil meal (P = 0.006). That is a 24-person crossover comparing walnuts against olive oil in a single meal; it is not evidence of a 1.4-point chronic improvement, and it was never a meta-analysis, though it is frequently cited as one.

Back to Table of Contents

Mechanism: Inflammation, CRP, and Oxidative Stress

Chronic low-grade inflammation is a central driver of atherosclerotic cardiovascular disease, as established by the CANTOS trial (canakinumab anti-IL-1-beta therapy reduced cardiovascular events independent of LDL lowering) and the broader inflammation hypothesis of atherosclerosis. C-reactive protein (CRP, high-sensitivity assay) is the most-used clinical marker.

This is where the walnut literature does not deliver, and you should know it. The claim that nuts meaningfully lower inflammatory markers is widespread and is not supported by the pooled trial data.

Neale and colleagues (2017) systematically reviewed 32 randomized controlled trials of tree nuts and peanuts. Across 26 strata from 25 studies, nut consumption produced a small, non-significant difference in C-reactive protein: a weighted mean difference of −0.01 mg/L (95% CI −0.06 to 0.03). That is effectively zero, and it is one-fiftieth the size of the "0.5 to 1 mg/L reduction" that circulates in nutrition writing — a figure an earlier version of this page repeated. Their sensitivity analyses suggested even that flat result was influenced by two individual studies. Small, non-significant differences were likewise found for the other inflammatory biomarkers examined, including interleukin-6, TNF-alpha, and the adhesion molecules ICAM-1 and VCAM-1. The 2024 walnut-specific review reached the same conclusion for ICAM-1 and VCAM-1.

The reviewers' own summary: "Non-significant changes in other biomarkers indicate a lack of consistent evidence for effects of nut consumption on inflammation." It is worth adding that two of those authors declared funding or non-financial support from the California Walnut Commission and Nuts for Life — industry ties that would, if anything, bias toward a positive result. The null finding survived them.

The mechanistic story usually told here — ALA-derived resolvins and protectins, polyphenol inhibition of NF-kB, urolithin-A-driven mitophagy in macrophages — is real cell and animal biology. It has simply not translated into a measurable anti-inflammatory effect in humans eating nuts. Treat it as a hypothesis for why walnuts might help, not as a demonstrated mechanism for why they do.

Back to Table of Contents

Mechanism: Blood Pressure and Vascular Stiffness

Walnut intervention produces modest blood pressure reductions in trials — typically 2-4 mmHg systolic and 1-2 mmHg diastolic with daily 30-60 g consumption. The effect is smaller than what is achieved with DASH diet adherence or sodium restriction but contributes incrementally.

The mechanisms include endothelial NO-mediated vasodilation (discussed above), reduction in arterial stiffness measured by pulse wave velocity, and modest natriuresis from the increased dietary potassium and magnesium delivered by walnuts (about 125 mg potassium and 45 mg magnesium per ounce).

For patients with stage 1 hypertension (130-139/80-89 mmHg), walnut intervention is a reasonable dietary component alongside DASH dietary pattern, sodium restriction, weight loss if overweight, and adequate dietary potassium. For higher-stage hypertension requiring pharmacological treatment, walnuts contribute incremental benefit but do not replace drug therapy.

Back to Table of Contents

Mechanism: Atrial Fibrillation and Arrhythmia

Atrial fibrillation is the most common sustained cardiac arrhythmia and a major cause of stroke, so a diet that prevented it would matter enormously. PREDIMED did produce a significant atrial fibrillation finding — and it belongs to the olive-oil arm, not the nuts arm.

Martínez-González and colleagues (2014) followed the 6,705 PREDIMED participants who did not have atrial fibrillation at randomization. Over a median 4.7 years there were 72 new cases in the olive-oil group, 82 in the nuts group, and 92 in the control group:

We are flagging this deliberately, because an earlier version of this page reported the result the wrong way round — attributing the 38% reduction to the nuts arm and stating that the olive-oil arm showed no benefit. That is the exact opposite of what the trial found, and the mistake is common enough in nut-related writing that it is worth naming. The paper is titled "Extravirgin olive oil consumption reduces risk of atrial fibrillation," and it says what its title says.

Two further limits on even the olive-oil finding: the analysis was post hoc, meaning atrial fibrillation was not a pre-specified endpoint of PREDIMED, and the authors framed their own conclusion as a suggestion rather than a demonstration — extra-virgin olive oil "may reduce the risk of atrial fibrillation."

Bottom line for walnuts: there is currently no trial evidence that walnuts prevent atrial fibrillation. The mechanistic arguments sometimes offered — ALA stabilizing atrial myocyte membranes, less atrial fibrosis, better atrial endothelial function — remain hypotheses, and PREDIMED is the largest test they have had. It came out null.

Back to Table of Contents

PREDIMED-Plus and the Weight-Loss Extension

The PREDIMED-Plus trial (still ongoing follow-up) extended the PREDIMED concept to a Mediterranean-diet-plus-physical-activity-plus-energy-restriction intervention in overweight or obese adults with metabolic syndrome. The primary endpoint is again hard cardiovascular events. Interim analyses have shown:

PREDIMED-Plus is testing whether the Mediterranean pattern combined with deliberate weight loss and exercise produces cardiovascular benefit beyond what PREDIMED showed. Recruitment finished in 2019 and follow-up continues; the primary cardiovascular result has been "expected soon" for several years now, so treat any claim about what it will show as speculation.

Back to Table of Contents

Practical Recommendations

Practical translation of PREDIMED and the broader walnut-and-cardiovascular literature:

For broader cardiovascular dietary intervention, see our Mediterranean Diet page and the Cardiology category.

Back to Table of Contents

Cautions

Back to Table of Contents

Key Research Papers

Every citation below has been checked against the PubMed record and links to a specific paper by its PMID, so you can verify the journal, year, volume and author list yourself. Where an earlier version of this page cited a paper by a PubMed keyword search, that link has been replaced — a search link cannot be checked, and three of the twelve turned out to carry the wrong author or the wrong year.

  1. Estruch R, Ros E, Salas-Salvadó J, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. New England Journal of Medicine. 2013;368(14):1279-1290. This paper was retracted in 2018; it is listed because it is the version most often quoted. Cite the 2018 republication instead. — PMID 23432189
  2. 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. New England Journal of Medicine. 2018;378(25):e34. The corrected re-publication, and the authoritative version. — PMID 29897866
  3. Rees K, Takeda A, Martin N, et al. Mediterranean-style diet for the primary and secondary prevention of cardiovascular disease. Cochrane Database of Systematic Reviews. 2019;3:CD009825. The independent appraisal: little or no effect on cardiovascular or total mortality, a real reduction in stroke, evidence graded low to moderate quality. — PMID 30864165
  4. Martínez-González MÁ, Toledo E, Arós F, et al. Extravirgin olive oil consumption reduces risk of atrial fibrillation: the PREDIMED trial. Circulation. 2014;130(1):18-26. The olive-oil arm reduced atrial fibrillation; the nuts arm did not. — PMID 24787471
  5. Banel DK, Hu FB. Effects of walnut consumption on blood lipids and other cardiovascular risk factors: a meta-analysis and systematic review. American Journal of Clinical Nutrition. 2009;90(1):56-63. Thirteen trials, 365 participants. — PMID 19458020
  6. Sabaté J, Oda K, Ros E. Nut consumption and blood lipid levels: a pooled analysis of 25 intervention trials. Archives of Internal Medicine. 2010;170(9):821-827. — PMID 20458092
  7. Neale EP, Tapsell LC, Guan V, Batterham MJ. The effect of nut consumption on markers of inflammation and endothelial function: a systematic review and meta-analysis of randomised controlled trials. BMJ Open. 2017;7(11):e016863. Thirty-two trials; no significant effect on C-reactive protein or other inflammatory markers. — PMID 29170286
  8. Hsu CY, Alzahrani AA, Maabreh HG, et al. Effect of walnut consumption on markers of endothelial function in adults: a systematic review and meta-analysis of randomized controlled trials. Phytotherapy Research. 2024;38(3):1358-1366. Flow-mediated dilation improved by 0.94 percentage points; ICAM-1 and VCAM-1 did not change. — PMID 38200617
  9. Cortés B, Núñez I, Cofan M, et al. Acute effects of high-fat meals enriched with walnuts or olive oil on postprandial endothelial function. Journal of the American College of Cardiology. 2006;48(8):1666-1671. A 24-person crossover of a single test meal — not a meta-analysis, though widely cited as one. — PMID 17045905
  10. Ros E, Núñez I, Pérez-Heras A, et al. A walnut diet improves endothelial function in hypercholesterolemic subjects: a randomized crossover trial. Circulation. 2004;109(13):1609-1614. — PMID 15037535
  11. Ma Y, Njike VY, Millet J, et al. Effects of walnut consumption on endothelial function in type 2 diabetic subjects: a randomized controlled crossover trial. Diabetes Care. 2010;33(2):227-232. An earlier version of this page attributed this trial to Guasch-Ferré and dated it 2017; both were wrong. — PMID 19880586
  12. Bao Y, Han J, Hu FB, et al. Association of nut consumption with total and cause-specific mortality. New England Journal of Medicine. 2013;369(21):2001-2011. An observational cohort study, not a trial — it cannot establish causation. — PMID 24256379
  13. Salas-Salvadó J, Fernández-Ballart J, Ros E, et al. Effect of a Mediterranean diet supplemented with nuts on metabolic syndrome status: one-year results of the PREDIMED randomized trial. Archives of Internal Medicine. 2008;168(22):2449-2458. Published in 2008, not 2011 as previously listed here. — PMID 19064829
  14. Salas-Salvadó J, Díaz-López A, Ruiz-Canela M, et al. Effect of a lifestyle intervention program with energy-restricted Mediterranean diet and exercise on weight loss and cardiovascular risk factors: one-year results of the PREDIMED-Plus trial. Diabetes Care. 2019;42(5):777-788. — PMID 30389673
  15. Salas-Huetos A, Moraleda R, Giardina S, et al. Effect of nut consumption on semen quality and functionality in healthy men consuming a Western-style diet: a randomized controlled trial. American Journal of Clinical Nutrition. 2018;108(5):953-962. — PMID 30475967

PubMed Topic Searches

Back to Table of Contents

Connections

Back to Table of Contents