Pecans: Insulin and Metabolic Health

Table of Contents

1. Insulin, HOMA-IR and Beta-Cell Function in Plain Words
2. The Tufts Feeding Trial: Insulin and HOMA-IR
3. The Eight-Week Trials in Adults at Cardiovascular Risk
4. Four Weeks in Healthy Older Adults: A Null Result on Glucose
5. Single-Meal Studies: Pecans Versus a Starchy Snack
6. People With Coronary Artery Disease
7. Body Weight, Body Fat and Energy Expenditure
8. Appetite Hormones and Fullness
9. What the Nut-and-Diabetes Meta-Analyses Found
10. Possible Mechanisms (Hypotheses)
11. What Is Not Known
12. Who the Research Raises Concerns For
13. Connections
14. Key Research Papers
15. Featured Videos

Insulin, HOMA-IR and Beta-Cell Function in Plain Words

Almost every pecan trial reports the same handful of blood measurements. They are worth understanding before reading the results, because a change in one of them is not the same thing as a change in disease risk.

• Fasting glucose is the sugar level in the blood after an overnight fast. It is the number used to diagnose prediabetes and type 2 diabetes, but it often stays normal for years while the body is working harder and harder to keep it there.
• Fasting insulin is the amount of insulin the pancreas has to release to hold that glucose steady. A rising fasting insulin with a normal glucose is the classic early sign of insulin resistance.
• HOMA-IR (Homeostasis Model Assessment of Insulin Resistance) is a calculation from fasting glucose and fasting insulin. Higher values mean more insulin is needed per unit of glucose control — that is, more insulin resistance.
• HOMA-β is a companion calculation from the same two numbers, intended to estimate how hard the insulin-making beta cells of the pancreas are working. It is easy to misread: when fasting insulin falls while glucose stays the same, HOMA-β also falls. Researchers usually read that as the beta cells being under less strain, not as the beta cells failing.
• Post-meal (postprandial) glucose and insulin are measured by drawing blood repeatedly for a few hours after a test meal, and are often summarised as the area under the curve.
• The triglyceride-glucose (TyG) index combines fasting triglycerides and fasting glucose into one number that tracks insulin resistance.

All of these are surrogate markers. A trial that moves them for four or eight weeks shows that a food changes metabolism in the short term. It does not show that the food prevents diabetes, which would need trials lasting years and counting new diagnoses. No such trial exists for pecans.

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The Tufts Feeding Trial: Insulin and HOMA-IR

The trial most often cited for pecans and insulin was run at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University in Boston and published by McKay and colleagues in 2018. Its design is stricter than most nut studies, which is why it carries weight despite its size.

Design

• Who: 26 men and postmenopausal women aged 45 or older, all overweight or obese (body mass index 25 to 35) with fat carried around the waist. People with diabetes, cardiovascular disease or other endocrine disorders were excluded, so this was a group at metabolic risk but not yet diagnosed.
• Design: a randomised, controlled crossover feeding trial — each person ate both diets in random order, with a two-week run-in, two four-week feeding periods and a two-week washout between them. All meals were prepared in the research kitchen and provided to participants.
• Diets: the control diet was built to resemble a typical American diet — low in fruit, vegetables and fiber, high in calorie-dense, nutrient-poor foods. On the pecan diet, whole pecans replaced 15 percent of total calories (about 42.5 grams, or roughly 1.5 ounces, per 2,000 kcal). The two diets were matched for total fat and fiber, and calories were set to keep body weight steady. That matching matters: any difference could not be put down to simply eating more fat or more fiber.

Results

After four weeks, compared with the control diet, the changes in serum insulin, HOMA-IR and HOMA-β were all significantly greater on the pecan diet. The full paper's results table gives the size of those changes:

• Fasting insulin (average 12.9 µIU/mL at the start) fell by 1.31 on the pecan diet and rose by 0.69 on the control diet — a between-diet difference of 2.0 µIU/mL.
• HOMA-IR (average 3.2 at the start) fell by 0.31 on pecans and rose by 0.20 on control — a difference of about 0.5.
• HOMA-β fell by about 16 units on pecans and rose by about 6 on control. Read alongside the lower insulin, the authors interpreted this as the beta cells needing to secrete less insulin to keep glucose in range.
• Fasting glucose barely moved (down about 1 mg/dL on pecans, up about 0.5 on control) and the difference was not statistically significant. The insulin change happened without a glucose change, which is what an improvement in insulin sensitivity in a not-yet-diabetic group would look like.
• Total and LDL cholesterol were lower after the pecan diet relative to control, but the differences were of borderline significance (p = 0.056 and 0.067). Blood pressure did not differ significantly, and body weight did not change.
• A composite score combining insulin, glucose, total cholesterol, LDL and triglycerides fell by 0.14 standard deviations on pecans and rose by 0.25 on control (difference p = 0.009). The authors described this as a concurrent and clinically significant effect on several markers of cardiometabolic risk.

Two further details from the full paper are useful. Red blood cell levels of oleic acid — the main fat in pecans — rose on the pecan diet, which confirms that people ate the pecans. And the control diet's worsening (insulin, cholesterol and LDL all drifted up on it) contributes to the between-diet differences; part of the “pecan effect” is the gap between pecans and a deliberately poor American-style diet. The full text is open at PubMed Central (PMC5872757).

What it does not show: 26 people, four weeks per diet, surrogate markers only. It shows that, in a controlled setting, swapping some calories for pecans lowered fasting insulin in people with central obesity. It does not show prevention of type 2 diabetes.

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The Eight-Week Trials in Adults at Cardiovascular Risk

A research group led by Cooper at the University of Georgia then ran a larger, longer and less controlled trial. Participants lived at home and ate their own food. The 2021 report by Guarneiri and colleagues randomised 56 adults who either had a body mass index of 28 or higher or had high cholesterol into three groups for eight weeks:

• Control (18 people): no nuts.
• ADD (16 people): 68 grams of pecans a day (about 2.4 ounces, around 470 kcal) added to their usual diet with no instructions to eat less of anything else.
• SUB (18 people): the same 68 grams a day, with instructions to substitute the pecans for foods of equal calories in their habitual diet.

At the start and after eight weeks, each person ate a high-fat test meal and had blood drawn over four hours. Fasting total cholesterol, LDL cholesterol, triglycerides, non-HDL cholesterol and apolipoprotein B fell in both pecan groups, with no changes in control. On the glucose side the abstract reports a single finding: a reduction in post-meal glucose in the SUB group (P < 0.05). It reports no change in fasting glucose or insulin. The lipid side of this trial is covered on Pecans: Cholesterol and Lipids.

Two further reports from the same eight-week programme looked at energy expenditure and at body weight; they are summarised under body weight and energy below.

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Four Weeks in Healthy Older Adults: A Null Result on Glucose

The same group then studied healthy adults aged 50 to 75. In the report by Cogan and colleagues (2023), 41 people were randomised to 68 grams of pecans a day (21 people) or a nut-free diet (20 people) for four weeks. Before and after, blood was drawn fasting and at 30, 60 and 120 minutes after a meal high in saturated fat.

There were no differences in fasting or post-meal glucose or insulin between the pecan and control groups. Post-meal lipid peroxidation (a marker of oxidative stress, covered on Pecans: Antioxidants and Oxidized LDL) was suppressed on pecans. The authors wrote that longer interventions, or a population with diabetes, may be needed to see effects on blood sugar regulation.

This null result is as important as the positive Tufts result. The obvious difference between them is the participants: the Tufts group was overweight or obese with central adiposity and an average starting HOMA-IR of 3.2, while this group was healthy. A food that improves insulin sensitivity is likely to show the clearest effect in people who have some insulin resistance to begin with — but that is a reading of two small trials, not a tested conclusion.

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Single-Meal Studies: Pecans Versus a Starchy Snack

Pecans or tortilla chips at mid-morning

Peters and colleagues (2024) ran a randomised crossover trial in 20 adults with overweight or obesity. Each person came in twice, had catheters placed for repeated blood sampling, ate a standardised breakfast, and two hours later ate a 250-kcal snack of either pecans or tortilla chips, followed by a lunch they chose themselves.

• Glucose and insulin rose significantly more after the tortilla chips.
• Free fatty acids, triglycerides and the gut hormones PYY (peptide YY) and GLP-1 (glucagon-like peptide-1) were higher after pecans.
• Subjective appetite, energy use, lunch intake and the make-up of lunch did not differ between the two snacks.

The authors concluded that pecans improve post-meal glucose and insulin profiles compared with a high-carbohydrate snack, and that whether the higher PYY and GLP-1 affect appetite and intake over the long term needs further study. The comparison is a fair one for real life, since a handful of nuts usually replaces another snack, but it is a comparison against chips, not against nothing. (GLP-1 is the same gut hormone that the newer weight-loss drugs imitate; see the GLP-1 and incretin animation. The rise after a snack of pecans is a normal digestive response and is not comparable in size or duration to a drug.)

A pecan breakfast shake versus a matched shake

Prater, Guadagni and Cooper (2024) ran a double-blinded randomised crossover trial in 32 young, healthy, normal-weight adults (average age 22, body mass index 22.9); 31 completed it. On separate days they drank a breakfast shake containing 68 grams of pecans (795 kcal) or a control shake matched for calories and macronutrients (794 kcal). Glucose and insulin were not the focus. After the pecan meal there was a greater overall PYY response, greater suppression of the hunger hormone ghrelin after two hours, greater fullness, and lower overall appetite reported at home 4 to 13 hours later. Self-reported calorie intake for the rest of the day did not differ.

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People With Coronary Artery Disease

The only pecan trial in the pack that included people treated for diabetes is a Brazilian trial in people with stable coronary artery disease. It is also the largest pecan trial to date. Dos Santos and colleagues (2022) randomised 204 patients for 12 weeks to one of three arms:

• a healthy diet alone (67 people);
• the healthy diet plus 30 grams of pecans a day (68 people);
• the healthy diet plus 30 mL of extra-virgin olive oil a day (69 people).

The primary outcome was the triglyceride-glucose index. After adjustment for baseline values and for use of diabetes drugs and insulin, there were no differences between groups in any glycemic measure or in body-fat-distribution indexes at the end of the study. The pecan group did end with a higher diet-quality score (modified Alternate Healthy Eating Index: 26 in the pecan group, against 19 in control and 18.9 in the olive oil group).

A companion report from the same trial (Weschenfelder and colleagues, 2022) found no significant effect of pecans or olive oil on inflammatory markers; interleukin-6, the primary outcome, fell in all three groups including control.

Two things limit what this trial can say about insulin. All three groups were already on a healthy diet, so the pecan arm was being compared with an already improved diet, not with a poor one. And the abstract does not report how many participants had diabetes, only that drug and insulin use was adjusted for. No pecan trial in the pack enrolled people with diagnosed type 2 diabetes as its target group, and none measured HbA1c (the long-term blood sugar test; see Hemoglobin A1C).

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Body Weight, Body Fat and Energy Expenditure

A daily 68-gram portion of pecans adds roughly 470 kcal. Simple arithmetic predicts weight gain if nothing else changes. The trials consistently found much less than that.

Eight weeks, with and without instructions to substitute

Guarneiri and colleagues (2022, Journal of Nutritional Science) reported body weight and body fat from the University of Georgia programme, with a nut-free control group (32 people), an ADD group (30) and a SUB group (31), each pecan group eating 68 grams a day for eight weeks.

• Body weight rose in all three groups. The rise was 1.1 kg in ADD and 0.9 kg in SUB against 0.3 kg in control — a trend that did not reach statistical significance (P = 0.09).
• The predicted gain, had the pecan calories simply been added with no compensation, was 3.3 kg in ADD and 3.2 kg in SUB. Actual gain was about a third of that (P < 0.001).
• Body fat percentage rose by 1.0 percentage point in the SUB group (P = 0.005), but not in ADD (0.1) or control (−0.2). This is an unexpected result — the group told to substitute gained body fat while the group simply adding pecans did not — and the abstract offers no explanation.

The authors concluded that daily pecan consumption for eight weeks did not result in significant weight gain, regardless of substitution instructions.

Four weeks in older adults

In the older-adult trial (Cogan and colleagues, 2023, Clinical Nutrition ESPEN; 44 people, 68 grams a day), body weight and body fat did not change in either group. Predicted gain on pecans was 2.2 kg; actual gain was 0.4 kg.

The Tufts trial

Calories were controlled to hold weight steady and, as intended, no significant weight change occurred. This trial says nothing about weight, but it does mean its insulin result was not a side effect of weight loss.

Energy expenditure and fat burning

A third report from the eight-week programme (Guarneiri and colleagues, 2022, Journal of Human Nutrition and Dietetics) measured metabolism by indirect calorimetry — analysing breathed air to calculate calories burned and the mix of fat and carbohydrate being used — while fasting and for four hours after a high-saturated-fat meal. Of 56 sedentary adults randomised, 47 completed the trial.

• In the SUB group, fasting resting metabolic rate rose from 1,607 to 1,701 kcal a day, fasting fat oxidation rose, and the respiratory exchange ratio fell (a shift toward burning fat).
• In the ADD group, diet-induced thermogenesis — the extra calories burned digesting a meal — rose after the test meal.
• There were no differences between groups for any outcome, and no changes within the control group. The within-group changes are suggestive; the trial did not show that pecans raised energy expenditure compared with not eating them.

The general picture matches the wider nut literature: weight changes after adding nuts are smaller than the calorie count predicts. A 2025 review of pecan research (Sandhu and colleagues) described body-weight changes after pecan intake as neutral. Part of the explanation proposed for nuts in general is that some of the fat stays locked inside intact plant cell walls and is never absorbed, and part is that nuts reduce how much of other foods people eat; the pecan trials above were not designed to separate those. More on the broader question is on Obesity.

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Appetite Hormones and Fullness

Several trials measured the gut hormones that signal fullness (PYY, CCK, GLP-1) and the hormone that signals hunger (ghrelin). These matter for metabolic health because appetite regulation is one route by which a food could affect body weight and, through it, insulin resistance.

• Eight weeks, adults at cardiovascular risk (Guarneiri and colleagues, 2022, Appetite; control 16, ADD 15, SUB 16; 68 g a day): within the ADD group, post-meal CCK and PYY rose and post-meal ghrelin was suppressed from before to after the intervention, but there were no differences between groups in these hormones. Across the whole day, the fall in “prospective consumption” and “desire to eat” ratings was greater in ADD than in SUB or control (p = 0.05 for both comparisons). Self-reported energy intake did not change.
• Four weeks, healthy older adults (Cogan and colleagues, 2023; pecan 21, control 23): fasting PYY rose from 77.0 to 93.5 pg/mL on pecans while it fell slightly from 76.0 to 72.5 on control (p = 0.01), and post-meal PYY also rose more on pecans (p = 0.04). CCK and ghrelin did not differ. Most subjective appetite ratings did not differ, though peak “desire to eat” was suppressed on pecans (p = 0.04). At a laboratory buffet, intake rose by 137 kcal in control and fell by 45 kcal on pecans, a trend that was not statistically significant (p = 0.11).
• Single meals: the two crossover studies above both found higher PYY after pecans; one also found higher GLP-1 and the other greater ghrelin suppression and fullness. Neither found a difference in how much people ate afterwards.

Put together: pecans fairly consistently raise PYY, the evidence on subjective appetite is mixed, and no trial has yet shown that people eat measurably less overall. The 2025 review by Sandhu and colleagues summarised the satiety-peptide results as promising.

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What the Nut-and-Diabetes Meta-Analyses Found

No meta-analysis has pooled pecan trials on their own — there are too few. The relevant pooled evidence is for nuts as a group, and most of it is observational: studies that recorded what people ate and followed them for years to see who developed diabetes or obesity.

Type 2 diabetes: no clear association for nuts

Schwingshackl and colleagues (2017) carried out a systematic review and dose-response meta-analysis of prospective studies on 12 food groups and type 2 diabetes. In the abstract, nuts were not among the six food groups with a significant link; the authors graded the meta-evidence for nuts as “low”. The full paper (open at PubMed Central, PMC5506108) gives the numbers:

• Eight studies with 27,016 cases of type 2 diabetes, intakes ranging from 0 to 27 grams a day.
• Highest versus lowest nut intake: relative risk 0.95 (95% confidence interval 0.85 to 1.05) — not statistically significant, with high heterogeneity between studies.
• Each additional 28 grams a day: relative risk 0.89 (0.71 to 1.12) — also not significant.
• A significant inverse association appeared in the subgroup of studies from Asian countries and in studies with shorter follow-up.

Banjarnahor and colleagues (2025) published an umbrella review — a review of the meta-analyses themselves — covering 13 food groups and the risk of type 2 diabetes and metabolic syndrome, from 67 articles. Whole grains (and, as a tendency, fruits and vegetables) were associated with lower risk; processed meat, red meat and sugar-sweetened beverages with higher risk. For the remaining food groups, which include nuts, the associations were generally neutral and not statistically significant, and heterogeneity was high for most groups.

Overweight and obesity: an inverse association

Kristoffersen and colleagues (2025) ran a companion umbrella review on food groups and the risk of overweight and obesity. Nuts had the largest data set of any food group: 520,331 participants and 91,256 cases. High intakes of whole grains, legumes, nuts and fruits were associated with a reduced risk of overweight and obesity. Heterogeneity was high for most food groups, and these are associations, not proof that nuts prevent weight gain.

A controlled comparison in metabolic syndrome

Galié and colleagues (2021) randomised 50 adults with metabolic syndrome to a crossover trial of two months on a Mediterranean diet and two months eating 50 grams of nuts a day on top of their usual non-Mediterranean diet, with a one-month washout. Glucose, insulin and HOMA-IR fell more after the Mediterranean diet than after the nut period. In this trial, adding nuts to an otherwise unchanged diet did less for insulin than changing the whole diet.

The honest summary is that the population-level evidence linking nuts to lower diabetes risk is weak and inconsistent, the evidence linking nuts to lower obesity risk is more consistent but observational, and the short-term pecan trials on insulin point in different directions. A broader overview of nuts as a group is on Nut Benefits.

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Possible Mechanisms (Hypotheses)

None of the explanations below has been tested directly in a pecan trial. They are the reasons researchers give for why pecans might affect insulin and metabolism, and they are listed as hypotheses.

1. Very little digestible carbohydrate. According to US Department of Agriculture data summarised on the main Pecans page, a 28-gram handful contains about 3.9 grams of carbohydrate, of which 2.7 grams is fiber. When pecans replace a starchy snack, the meal simply delivers less glucose — the most direct explanation for the tortilla-chip result above.
2. The fat profile. Most of the fat in a pecan is the monounsaturated oleic acid that dominates olive oil. In the Tufts trial, red blood cell oleic acid rose and palmitic acid (a saturated fat) fell on pecans. Replacing saturated fat with unsaturated fat is thought to improve insulin signalling in muscle and liver cells; in these trials that link is a hypothesis.
3. Fiber. About 9.6 grams per 100 grams. Fiber slows digestion and feeds gut bacteria. In the Tufts trial the control diet was matched for fiber using added wheat bran, so fiber alone does not explain that result.
4. Magnesium. Insulin needs magnesium to work inside cells, and low magnesium intake is linked to insulin resistance in observational research. A handful of pecans gives about 34 mg, roughly 8 percent of the Daily Value — a modest amount. No pecan trial has measured magnesium status.
5. Manganese. Pecans are an exceptionally rich source — about 1.3 mg per handful, more than half the Daily Value. Manganese is a cofactor for enzymes involved in carbohydrate metabolism and for the mitochondrial antioxidant enzyme manganese superoxide dismutase. Whether pecan manganese plays any role in the insulin findings is unknown.
6. Polyphenols. Pecans are unusually rich in tannins, flavan-3-ols and proanthocyanidins (reviewed by Bolling and colleagues, 2011). A 2024 systematic review by Farazi and colleagues found that polyphenol-rich extracts from several nuts, including pecan, inhibited the starch-digesting enzyme α-amylase in test-tube studies using pig pancreatic enzyme. Only four of the 31 studies it reviewed used human enzymes, and the authors cautioned that pig and especially microbial enzymes do not reliably predict effects in people. This is laboratory evidence only.
7. Gut hormones. The higher PYY and GLP-1 seen after pecan meals could in principle slow stomach emptying and blunt the glucose rise. That has not been shown to explain any long-term change.
8. Displacement. In free-living trials, pecans replace other foods. What they replace — often refined carbohydrate — may matter as much as what they contain. The Brazilian trial, in which the pecan group's diet-quality score rose, illustrates this side of the effect.

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What Is Not Known

• Whether pecans prevent or delay type 2 diabetes. No trial has counted new diagnoses. The longest pecan trial lasted 12 weeks.
• Whether the Tufts insulin result replicates. It came from 26 people in a fully controlled feeding study. The later free-living trials did not report the same change in fasting insulin, and the older-adult trial found none.
• What pecans do in people with diagnosed type 2 diabetes. No pecan trial has targeted this group or measured HbA1c.
• Which part of the pecan matters. Fat, fiber, minerals, polyphenols and displacement have not been separated.
• The best comparison. Results depend heavily on what pecans are compared with: a poor American-style diet (Tufts), a nut-free diet (Georgia), tortilla chips (Colorado), or an already healthy diet (Brazil). A benefit against chips is not a benefit against an apple.
• Dose. Trials used about 30, 42.5 or 68 grams a day. None compared doses.
• Long-term weight. The weight results cover four to eight weeks. The observational evidence on nuts and obesity points in a favourable direction, but it is observational.
• Generalisability. Most of the trials come from a few research groups (in Georgia, Massachusetts, Colorado and southern Brazil) and enrolled small samples; how far the results extend to other populations and diets is untested.

The 2025 review by Sandhu and colleagues reached a similar overall view: replacing foods and snacks with pecans improves diet quality and lipid profiles, while effects on glycemia, vascular function and inflammation are inconsistent.

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Who the Research Raises Concerns For

• People with tree-nut allergy. Pecans are a tree nut and are closely related to walnuts. People with nut allergy were excluded from the trials above, which therefore say nothing about them.
• People counting calories. The 68-gram daily amount used in several trials is about 470 kcal. In the eight-week trial, weight rose by about 1 kg in both pecan groups and body fat rose in the substitution group. Smaller weight gain than predicted is not the same as no weight gain.
• People taking glucose-lowering medicines. The trials found pecans to be neutral or modestly favourable for glucose; none of the abstracts reports on hypoglycaemia (low blood sugar). Changes in diet alongside diabetes medicines are a question for the prescribing clinician.
• Sweetened pecan products. All of the trials used plain pecans. Candied, praline or glazed pecans and pecan pie are largely sugar, and none of the findings on this page applies to them.

Decisions about diet in diabetes, prediabetes or insulin resistance belong with a clinician who knows the person's full picture.

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Connections

• Nuts — all the nuts on the site
• Pecans — the main pecan page
• Pecans — Benefits Deep Dive — the hub for these articles
• Pecans: Cholesterol and Lipids — the lipid side of the same trials
• Pecans: Antioxidants and Oxidized LDL — polyphenols and post-meal oxidation
• Nut Benefits — the evidence for nuts as a group
• Insulin Resistance — what HOMA-IR is tracking
• Metabolic Syndrome — the cluster these trials are aimed at
• Prediabetes — the stage before diagnosis
• Type 2 Diabetes — the disease itself
• Obesity — weight and body fat
• HOMA-IR — the calculation explained
• Fasting Insulin — the test behind it
• Manganese — the mineral pecans are richest in
• Magnesium — insulin's mineral partner
• Pistachios — another nut studied for blood sugar
• Almonds — the most-studied tree nut

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Key Research Papers

1. McKay DL, Eliasziw M, Chen CYO, et al. A Pecan-Rich Diet Improves Cardiometabolic Risk Factors in Overweight and Obese Adults: A Randomized Controlled Trial. Nutrients. 2018;10(3):339. PubMed PMID: 29534487
2. Guarneiri LL, Paton CM, Cooper JA. Pecan-Enriched Diets Alter Cholesterol Profiles and Triglycerides in Adults at Risk for Cardiovascular Disease in a Randomized, Controlled Trial. The Journal of nutrition. 2021;151(10):3091-3101. PubMed PMID: 34383903
3. Cogan B, Pearson RC, Jenkins NT, et al. A 4-Week Pecan-Enriched Diet Improves Postprandial Lipid Peroxidation in Aging Adults. Journal of medicinal food. 2023;26(9):654-662. PubMed PMID: 37638838
4. Peters JC, Breen JA, Pan Z, et al. A Randomized, Crossover Trial Assessing Appetite, Energy Metabolism, Blood Biomarkers, and Ad Libitum Food Intake Responses to a Mid-Morning Pecan Snack vs. an Equicaloric High-Carbohydrate Snack in Healthy Volunteers with Overweight/Obesity. Nutrients. 2024;16(13):2084. PubMed PMID: 38999832
5. Prater MC, Guadagni AJ, Cooper JA. Postprandial appetite responses to a pecan enriched meal: A randomized crossover trial. Appetite. 2024;201:107598. PubMed PMID: 38971424
6. Dos Santos JL, Portal VL, Markoski MM, et al. Effect of pecan nuts and extra-virgin olive oil on glycemic profile and nontraditional anthropometric indexes in patients with coronary artery disease: a randomized clinical trial. European journal of clinical nutrition. 2022;76(6):827-834. PubMed PMID: 34811509
7. Weschenfelder C, Gottschall CBA, Markoski MM, et al. Effects of supplementing a healthy diet with pecan nuts or extra-virgin olive oil on inflammatory profile of patients with stable coronary artery disease: a randomised clinical trial. The British journal of nutrition. 2022;127(6):862-871. PubMed PMID: 33971993
8. Guarneiri LL, Paton CM, Cooper JA. Changes in body weight in response to pecan-enriched diets with and without substitution instructions: a randomised, controlled trial. Journal of nutritional science. 2022;11:e16. PubMed PMID: 35320927
9. Guarneiri LL, Paton CM, Cooper JA. Pecan-enriched diets increase energy expenditure and fat oxidation in adults at-risk for cardiovascular disease in a randomised, controlled trial. Journal of human nutrition and dietetics. 2022;35(5):774-785. PubMed PMID: 34841598
10. Guarneiri LL, Paton CM, Cooper JA. Appetite responses to pecan-enriched diets. Appetite. 2022;173:106003. PubMed PMID: 35307465
11. Cogan B, Pearson RC, Jenkins NT, et al. A pecan-enriched diet reduced postprandial appetite intensity and enhanced peptide YY secretion: A randomized control trial. Clinical nutrition ESPEN. 2023;56:25-35. PubMed PMID: 37344080
12. Sandhu AK, Edirisinghe I, Burton-Freeman B. Pecans and Human Health: Distinctive Benefits of an American Nut. Nutrients. 2025;17(23):3686. PubMed PMID: 41373975
13. Schwingshackl L, Hoffmann G, Lampousi AM, et al. Food groups and risk of type 2 diabetes mellitus: a systematic review and meta-analysis of prospective studies. European journal of epidemiology. 2017;32(5):363-375. PubMed PMID: 28397016
14. Banjarnahor RL, Javadi Arjmand E, Onni AT, et al. Umbrella Review of Systematic Reviews and Meta-Analyses on Consumption of Different Food Groups and Risk of Type 2 Diabetes Mellitus and Metabolic Syndrome. The Journal of nutrition. 2025;155(5):1285-1297. PubMed PMID: 40122387
15. Kristoffersen E, Hjort SL, Thomassen LM, et al. Umbrella Review of Systematic Reviews and Meta-Analyses on the Consumption of Different Food Groups and the Risk of Overweight and Obesity. Nutrients. 2025;17(4):662. PubMed PMID: 40004990
16. Galié S, García-Gavilán J, Camacho-Barcía L, et al. Effects of the Mediterranean Diet or Nut Consumption on Gut Microbiota Composition and Fecal Metabolites and their Relationship with Cardiometabolic Risk Factors. Molecular nutrition & food research. 2021;65(19):e2000982. PubMed PMID: 34331403
17. Farazi M, Houghton MJ, Cardoso BR, et al. Inhibitory effect of extracts from edible parts of nuts on α-amylase activity: a systematic review. Food & function. 2024;15(10):5209-5223. PubMed PMID: 38717256
18. Bolling BW, Chen CY, McKay DL, et al. Tree nut phytochemicals: composition, antioxidant capacity, bioactivity, impact factors. A systematic review of almonds, Brazils, cashews, hazelnuts, macadamias, pecans, pine nuts, pistachios and walnuts. Nutrition research reviews. 2011;24(2):244-75. PubMed PMID: 22153059

PubMed Topic Searches

1. Pecans and insulin, glucose or HOMA-IR
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3. Tree nuts and glycemic control: meta-analyses
4. Nut consumption and type 2 diabetes: randomised trials
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