Chia Seeds for ALA Omega-3

Chia seeds are the highest plant-source concentration of alpha-linolenic acid (ALA, the 18-carbon, 3-double-bond omega-3 precursor) of any commonly consumed food — roughly 17 g per 100 g of seed, or about 60% of total fat. That is more by weight than flax, perilla, or sacha inchi. ALA is the parent omega-3 from which the body synthesizes EPA (eicosapentaenoic acid, 20:5n-3) and DHA (docosahexaenoic acid, 22:6n-3) through a sequence of elongation and desaturation steps. Conversion efficiency is low (5-8% ALA to EPA, less than 1% to DHA in most adults), but a growing body of research suggests ALA itself has independent effects on cardiovascular risk independent of its role as EPA/DHA precursor. This page covers the biochemistry, the conversion limits, the cardiovascular trial evidence, the case for and against fish-oil supplementation, and practical positioning of chia within an omega-3 strategy for vegetarians, vegans, and omnivores who want a plant complement to (or replacement for) fish oil.

Table of Contents

1. What ALA Is (and Why It Matters)
2. Chia Versus Flax, Walnut, Perilla, and Sacha Inchi
3. The Conversion-Efficiency Problem (Delta-6-Desaturase)
4. ALA Has Independent Effects (Beyond Conversion)
5. The Lyon Diet Heart Study and the ALA Cardioprotection Signal
6. PREDIMED and the Mediterranean Diet Pattern
7. Blood Pressure Effects (Toscano 2014 Chia Trial)
8. Chia Versus Fish Oil: When Each Wins
9. The Vegan/Vegetarian Omega-3 Strategy
10. The Omega-6 to Omega-3 Ratio Problem
11. Practical Protocol: Dose, Form, Timing
12. Cautions and Drug Interactions
13. Key Research Papers
14. Connections

What ALA Is (and Why It Matters)

Alpha-linolenic acid (ALA, formally 18:3n-3 or cis,cis,cis-9,12,15-octadecatrienoic acid) is an 18-carbon polyunsaturated fatty acid with three double bonds, the first counting from the methyl end at position 3 — which is what makes it an "omega-3." It is one of two fatty acids classified as essential for humans (the other being linoleic acid, 18:2n-6, the omega-6 essential), meaning the body cannot synthesize it and must obtain it from diet. Without dietary ALA, the body cannot manufacture EPA and DHA at all, and clinical deficiency develops with neurological, dermatological, and immune consequences.

The body uses ALA in two ways. First, a small fraction is converted, through a sequence of desaturation and elongation steps catalyzed by the enzymes Delta-6-desaturase (encoded by FADS2), elongase ELOVL5, Delta-5-desaturase (FADS1), elongase ELOVL2, and a final peroxisomal beta-oxidation step, into the longer-chain omega-3s EPA (20:5n-3) and DHA (22:6n-3). These longer-chain omega-3s are then incorporated into cell membrane phospholipids and serve as substrates for the production of anti-inflammatory and pro-resolving eicosanoids (resolvins, protectins, maresins). Second, the ALA that is not converted is either beta-oxidized for energy or stored unchanged in adipose tissue triglycerides.

The minimum dietary requirement for ALA in adults, established by the Institute of Medicine, is approximately 1.6 g/day for men and 1.1 g/day for women (Adequate Intake values). Most Western diets fall short of even these modest amounts because the agricultural revolution has reduced ALA-rich foods (wild greens, grass-fed meat, flax, chia) and dramatically increased omega-6 vegetable oil consumption (soybean, corn, safflower, sunflower oils). A single 28 g serving of chia (one ounce, ~2 tablespoons) delivers approximately 4.9 g of ALA — roughly 3 times the minimum daily requirement — making chia one of the easiest ways to address dietary omega-3 inadequacy without animal products.

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Chia Versus Flax, Walnut, Perilla, and Sacha Inchi

Chia, flax, perilla, sacha inchi, and walnut are the five common plant foods that deliver clinically meaningful amounts of ALA. Per 100 g of food:

• Chia seeds: ~17 g ALA (~60% of total fat). High fiber, low oxalate, no cyanogenic glycosides, neutral flavor. The mucilage allows whole-seed consumption without grinding (in contrast to flax). Shelf-stable as whole seed for years due to high antioxidant content.
• Flax seeds (ground): ~22 g ALA (~57% of total fat). Higher ALA per gram than chia, but must be ground for digestion (whole flax passes intact) and ground flax oxidizes within weeks. Also contains lignans (phytoestrogens) with separate hormone-related effects.
• Perilla seed: ~58 g ALA per 100 g of oil; the dominant culinary omega-3 source in Korean and Japanese cuisine. Hard to source in Western markets; oil has very short shelf life.
• Sacha inchi (Plukenetia volubilis): ~48 g ALA per 100 g of seed. Peruvian "mountain peanut." Limited distribution and higher cost in North America.
• Walnuts: ~9 g ALA per 100 g (~14% of total fat). Much less concentrated than chia or flax but enjoyable as a whole food. Walnut linoleic acid content is roughly 4× walnut ALA, which dilutes the omega-3 effect when eaten in normal portions.

Practical comparison: a 28 g serving of chia gives ~4.9 g ALA. A 28 g serving of ground flax gives ~6.2 g ALA. A 28 g serving of walnuts (about a small handful, 7 halves) gives ~2.6 g ALA. Chia and flax are roughly interchangeable from an ALA standpoint; chia wins on shelf stability and digestibility without grinding, flax wins on lignan content and lower cost per gram of ALA. Many practitioners recommend rotating both for a broader phytonutrient profile.

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The Conversion-Efficiency Problem (Delta-6-Desaturase)

The single most important nuance in the ALA story is that conversion to EPA and DHA is inefficient in adult humans. The rate-limiting step is the first enzyme in the chain, Delta-6-desaturase (FADS2), which introduces a fourth double bond at position 6 to convert ALA (18:3n-3) to stearidonic acid (18:4n-3). The same enzyme also acts on the omega-6 pathway, converting linoleic acid (18:2n-6) to gamma-linolenic acid (18:3n-6) — and because typical Western diets contain 10-20 times more linoleic acid than ALA, the omega-6 substrate competes with and crowds out the omega-3 substrate at the enzyme's active site.

Stable-isotope tracer studies (Burdge and colleagues at the University of Southampton, summarized in Reproduction Nutrition Development 2005) have measured the conversion percentages with carbon-13-labeled ALA fed to volunteers. The pooled findings:

• ALA → EPA conversion: approximately 5-8% in women, 0-4% in men (women appear to have higher Delta-6-desaturase activity, possibly due to estrogenic upregulation supporting fetal brain DHA accumulation during pregnancy)
• ALA → DPA (22:5n-3): approximately 3-9%
• ALA → DHA: less than 1% in most adults, with some studies finding effectively zero conversion in adult men

Several factors modulate conversion. FADS1/FADS2 genetic variants account for substantial inter-individual variability — carriers of certain SNPs convert ALA at roughly twice the rate of non-carriers. High dietary linoleic acid intake competitively inhibits conversion. Insulin resistance and metabolic syndrome reduce Delta-6-desaturase activity. Conversely, low total energy intake, pregnancy, and lactation upregulate it.

The practical implication often quoted is that "ALA cannot fully replace EPA and DHA from fish for those targeting high circulating EPA/DHA levels (for example, after a cardiac event)." But the implication often missed is that ALA still produces meaningful clinical effects independent of conversion, covered in the next section.

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ALA Has Independent Effects (Beyond Conversion)

For roughly two decades, the prevailing view in cardiology was that ALA was useful only insofar as it converted to EPA/DHA, and that fish oil was therefore strictly superior. That view has shifted as multiple large prospective cohort studies and meta-analyses have shown that ALA intake independently predicts reduced cardiovascular events even after statistical adjustment for circulating EPA/DHA. Mechanisms that do not depend on conversion include:

• Membrane fluidity and arrhythmia threshold — ALA itself, before conversion, incorporates into cardiomyocyte membrane phospholipids and may directly modulate ion-channel function (particularly the late sodium current and the rapid delayed rectifier potassium current), reducing susceptibility to malignant ventricular arrhythmias. This is the proposed mechanism behind the dramatic sudden-cardiac-death reduction in the Lyon Diet Heart Study, where the intervention diet was rich in ALA from canola-oil margarine.
• Reduced platelet aggregation — ALA modestly inhibits platelet aggregation independent of conversion to EPA-derived thromboxane A3. The effect is smaller than aspirin's but is additive with low-dose aspirin.
• Blood pressure — ALA-rich diets reduce systolic blood pressure by approximately 3-4 mmHg in hypertensive patients (Toscano 2014 chia trial), comparable to a single low-dose antihypertensive medication. The mechanism appears to involve improved endothelial function via increased nitric oxide bioavailability.
• Anti-inflammatory effect on hepatic acute-phase proteins — ALA reduces serum C-reactive protein (CRP), interleukin-6, and tumor necrosis factor-alpha in clinical trials, suggesting genuine anti-inflammatory activity at the systemic level.
• Improved insulin sensitivity — observational and short-term interventional data suggest ALA improves whole-body insulin sensitivity, possibly via PPAR-alpha activation in hepatocytes.

The Pan et al. 2012 meta-analysis (American Journal of Clinical Nutrition) pooled 27 prospective cohort studies and found that each additional 1 g/day of dietary ALA was associated with approximately 10% lower risk of fatal cardiovascular disease. That effect size is independent of fish or EPA/DHA intake in the same models. For practical perspective: 28 g of chia delivers ~4.9 g of ALA, predicting a ~50% theoretical maximum reduction in fatal CVD risk if extrapolated linearly — though in reality dose-response curves plateau and the true marginal effect at higher intakes is smaller.

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The Lyon Diet Heart Study and the ALA Cardioprotection Signal

The Lyon Diet Heart Study (de Lorgeril et al., Circulation 1999) is the foundational randomized clinical trial that established ALA as cardioprotective. 605 patients who had survived a first myocardial infarction were randomized to either:

1. A Mediterranean-style diet with explicit ALA enrichment via canola-oil-based margarine (providing ~2 g ALA/day from the spread alone, plus background diet contributions)
2. Standard post-MI dietary advice from the patient's cardiologist (typically low-saturated-fat focused, with no specific omega-3 guidance)

The trial was stopped early at the recommendation of the safety monitoring board because of the magnitude of benefit in the intervention arm:

• ~70% reduction in cardiac death
• ~70% reduction in non-fatal MI
• ~56% reduction in all-cause mortality
• No difference in plasma lipid levels between arms (the benefit was not mediated by cholesterol change)

The benefit appeared too rapidly to be explained by atherosclerosis modification (effect emerged within weeks of randomization), suggesting an electrophysiologic anti-arrhythmic mechanism. Membrane phospholipid analysis showed substantially higher ALA, EPA, and DHA incorporation in the intervention group. The effect sizes are larger than for almost any pharmacologic intervention in secondary cardiovascular prevention, including statins, beta-blockers, and ACE inhibitors as single interventions.

The Lyon trial has been criticized for being underpowered for individual endpoints and for using a complex multi-component intervention that does not isolate the ALA effect from other Mediterranean-diet components (olive oil, fish, vegetables, modest red wine). But the magnitude and rapidity of effect have not been replicated by any other dietary intervention, and ALA enrichment was the single most distinctive feature of the intervention compared to standard care. The trial remains the strongest evidence that dietary ALA at intakes achievable through whole foods produces clinically meaningful cardiovascular benefit.

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PREDIMED and the Mediterranean Diet Pattern

The PREDIMED trial (Prevención con Dieta Mediterránea, Estruch et al. NEJM 2013 with corrections published 2018) is the largest randomized trial of a Mediterranean diet pattern. 7,447 high-cardiovascular-risk participants in Spain were randomized to one of three diets: Mediterranean diet plus extra-virgin olive oil supplementation, Mediterranean diet plus mixed nuts supplementation (15 g walnuts plus 7.5 g each almonds and hazelnuts daily), or a low-fat control diet.

Both Mediterranean-diet arms produced approximately a 30% reduction in the composite endpoint of myocardial infarction, stroke, and cardiovascular death over ~5 years of follow-up. The nut-supplemented arm provided substantial ALA (the walnut component is particularly ALA-rich), and substudies showed inverse association between plasma ALA concentration and event rate.

Substudies relevant to ALA include:

• Serum ALA and cardiovascular events — participants in the highest tertile of baseline plasma ALA had ~28% lower CVD events than the lowest tertile, after adjustment for olive oil and EPA/DHA intake
• Cognitive function — participants in the nut arm showed slowed cognitive decline over 4 years (Valls-Pedret et al. 2015)
• Atrial fibrillation — both Mediterranean arms had reduced incident atrial fibrillation, consistent with the proposed anti-arrhythmic effect of omega-3 fatty acids on cardiac electrophysiology

Although chia was not a study food in PREDIMED, it would substitute readily for walnuts in a similar diet pattern, delivering more ALA per gram and a more favorable omega-6 to omega-3 ratio (walnut is ~4:1 omega-6 to omega-3; chia is ~1:3 omega-6 to omega-3, i.e., already omega-3 dominant).

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Blood Pressure Effects (Toscano 2014 Chia Trial)

The Toscano et al. 2014 trial (Plant Foods for Human Nutrition) is the most cited clinical trial specifically of chia for blood pressure. 26 hypertensive subjects (some on antihypertensive medication, some untreated) were randomized to receive 35 g/day of chia flour (delivering approximately 6 g ALA), placebo flour, or chia flour in untreated hypertensives, for 12 weeks.

Results: the chia group showed:

• Systolic blood pressure reduction of approximately 4-6 mmHg over baseline, and approximately 6-11 mmHg over placebo (depending on subgroup)
• Diastolic blood pressure reduction of approximately 3-5 mmHg
• The blood-pressure effect was independent of medication status
• Notably, the effect was equivalent in subjects on antihypertensive medication and in unmedicated subjects, suggesting additive effect with pharmacotherapy
• The plasma ALA concentration approximately doubled in the chia group

For perspective, a 4-6 mmHg reduction in systolic blood pressure is in the same range as a low-dose ACE inhibitor or angiotensin receptor blocker, and is associated with approximately 20% lower stroke risk and 14% lower coronary event risk based on epidemiologic dose-response data. This is a non-trivial clinical effect from a food intervention with no drug interactions and no notable adverse effects.

Mechanistically, the blood-pressure effect appears to involve improved endothelial function (chia ALA increases endothelial nitric oxide synthase activity), reduced angiotensin-converting enzyme activity (in vitro and animal data), and possible direct vasodilatory effect of bioactive peptides released from chia protein during digestion. The trial did not separate these mechanisms, but the consistency with the broader ALA literature supports the endothelial-function explanation.

For more on hypertension management, see our Hypertension page.

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Chia Versus Fish Oil: When Each Wins

Chia and fish oil are not interchangeable. They occupy distinct niches in the omega-3 strategy, and the right choice depends on clinical context:

Fish oil (or fatty fish like sardines, mackerel, salmon, herring) wins when:

• Post-MI secondary prevention requires high circulating EPA/DHA (the GISSI-Prevenzione trial used 850 mg/day combined EPA+DHA)
• Severe hypertriglyceridemia (>500 mg/dL) requires prescription-strength omega-3 (Vascepa, Lovaza) at 2-4 g/day EPA ± DHA
• Direct DHA delivery to developing brain in pregnancy and infancy (DHA is the dominant phospholipid omega-3 in neural membranes; ALA conversion is insufficient to support fetal/infant CNS development)
• Documented EPA/DHA deficiency on RBC membrane fatty acid testing (omega-3 index <4%)
• Resolvin/protectin/maresin-mediated effects on chronic inflammatory disease (these specialized pro-resolving mediators are EPA/DHA-derived, not ALA-derived)

Chia (and other plant ALA) wins when:

• Vegetarian/vegan diet excludes fish (chia is the most efficient practical plant ALA source)
• Goal is general cardiovascular risk reduction in primary prevention (ALA confers most of the benefit at modest intakes, without requiring high circulating EPA/DHA)
• Hypertension management (the Toscano data are specifically for chia, not fish oil)
• Concern about heavy-metal contamination in fish or fish oil (chia has no mercury or PCBs)
• Concern about oxidative stability (whole chia seeds are stable at room temperature for 2-4 years due to high natural antioxidant content; fish oil oxidizes rapidly even refrigerated)
• Want the additional benefits of chia's fiber, calcium, and magnesium content (fish oil delivers only the fatty acids)

For most patients, the optimal strategy is both: 28 g chia daily delivers the baseline ALA load, complemented by 2-3 servings per week of fatty fish (or 500-1000 mg/day combined EPA+DHA from algal oil for vegans) to ensure adequate circulating EPA/DHA. The two are complementary rather than competing.

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The Vegan/Vegetarian Omega-3 Strategy

For strict vegans, fish and fish oil are off the table, and the question is how to ensure adequate omega-3 status from plants alone. The strategy has three components:

1. Maximize ALA intake — aim for 4-6 g/day of ALA, achievable with 28-35 g of chia or ground flax daily, or a combination. This is roughly 3-4× the IOM Adequate Intake target and ensures saturation of the conversion pathway.
2. Minimize omega-6 intake — the typical Western diet contains 10-20:1 omega-6 to omega-3 ratio; the goal is closer to 4:1 or less. Practically this means replacing soybean, corn, safflower, sunflower, and "vegetable" oils with olive oil, avocado oil, or culinary coconut oil; reducing reliance on commercial baked goods and fried foods cooked in omega-6-rich oils; and using nuts and seeds with naturally favorable ratios (chia, flax, walnut) rather than those with high omega-6 (sunflower seed, sesame, most almonds).
3. Consider direct DHA supplementation — vegan DHA derived from algae (the original source from which fish accumulate it through the food chain) is now widely available at 200-500 mg/day doses. Brands like Nordic Naturals Algae Omega, Ovega-3, Future Kind, and others offer EPA+DHA combinations from Schizochytrium sp. or Crypthecodinium cohnii algal cultures. This is particularly important during pregnancy, lactation, and infancy when DHA demand is high and conversion from ALA is insufficient.

Studies of long-term vegans show that ALA-only intake produces lower plasma and erythrocyte DHA concentrations than fish-eating omnivores, even when ALA intake is generous. The omega-3 index (a marker of cardiovascular risk based on RBC membrane EPA+DHA percentage) tends to run 2-3 percentage points lower in vegans than omnivores. Direct algal DHA closes this gap and produces omega-3 index values comparable to omnivores eating fish twice weekly.

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The Omega-6 to Omega-3 Ratio Problem

The absolute amount of ALA in the diet is only half the story. The omega-6 to omega-3 ratio determines how much of the ingested ALA actually makes it through the conversion pathway, because Delta-6-desaturase is shared between the two pathways. With excess linoleic acid (omega-6) flooding the enzyme, ALA conversion to EPA falls dramatically.

The estimated ratio in the ancestral human diet (paleolithic, based on archaeological food-residue analysis and modern hunter-gatherer studies) was approximately 1:1 to 4:1 omega-6 to omega-3. The current US population averages approximately 15-20:1. This shift is driven almost entirely by the industrial-scale production and consumption of soybean oil, which alone now accounts for over 60% of US edible oil consumption and is approximately 50:1 omega-6 to omega-3.

Adding chia to a diet without reducing omega-6 intake provides some benefit but is not optimal. The Lyon Diet Heart Study's extraordinary effect was almost certainly enhanced by the simultaneous reduction in omega-6 oils (the canola margarine that delivered the ALA also displaced soybean and corn oil from the diet). Practical steps to reduce the ratio:

• Replace soybean, corn, safflower, sunflower, and "vegetable" oils with olive oil for cooking
• Replace conventional commercial salad dressings (typically soybean-oil based) with homemade olive-oil dressings or commercial olive-oil-based brands
• Reduce frequency of restaurant and fast-food consumption (most restaurants use omega-6-rich oils for cost and shelf-stability reasons)
• Reduce ultra-processed snack foods (chips, crackers, baked goods are typically high-omega-6)
• Choose grass-fed or pasture-raised animal products where feasible (grain-finished animals have ~1:5 omega-3:omega-6 ratio; grass-finished are closer to 1:2)

A diet with reduced omega-6 plus added chia for omega-3 can shift the ratio toward 4:1 or better within weeks, which appears to be the threshold below which the anti-inflammatory and cardioprotective benefits become clinically apparent.

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Practical Protocol: Dose, Form, Timing

Dose: 28-35 g/day (1-1.25 oz, approximately 2-2.5 tablespoons) delivers ~5-6 g ALA, ~10-12 g fiber, and ~180 mg calcium. This is the dose used in most of the published clinical trials. Higher intakes (50-70 g/day) have been studied and are well tolerated but provide diminishing marginal benefit and increase fiber load that some individuals find uncomfortable.

Form:

• Whole seeds are well digested because the mucilage layer softens during gastric and small-intestinal transit, exposing the seed contents to enzymes. This is in contrast to flax, where the much harder seed coat causes whole flax to pass largely intact. Chia whole-seed digestibility studies (Vuksan group) show ALA bioavailability roughly 80% of ground-seed bioavailability — close enough that the practical convenience of whole seeds usually wins.
• Pre-soaked chia gel (chia + water in 1:9 ratio, allowed to gel for 10-30 minutes) maximizes mucilage hydration and is the traditional Tarahumara preparation (iskiate). Particularly useful for endurance applications and for individuals who find dry chia adds palatability concerns.
• Ground chia (chia flour) maximizes ALA bioavailability but oxidizes faster than whole seeds. Buy in small quantities and refrigerate.
• Chia oil delivers ALA without fiber or other co-nutrients. Useful when adding to existing high-fiber diets but loses the broader nutrient benefits of whole-seed chia.

Timing: any time of day. For blood-pressure benefit, divide between two meals to maintain a more constant plasma ALA. For postprandial glycemic effect (see the Soluble Fiber deep dive), consume immediately before or with meals containing carbohydrate. For endurance applications, see the Hydration and Endurance deep dive.

Storage: whole chia seeds in an airtight container in a cool dark place are stable for 2-4 years — the high antioxidant content of the seed coat prevents lipid oxidation. Ground chia and chia oil are more vulnerable: refrigerate and use within 1-3 months.

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Cautions and Drug Interactions

• Esophageal obstruction with dry chia — isolated case reports describe esophageal impaction when a tablespoon or more of dry chia is consumed followed immediately by water, because the seeds gel in the esophagus before reaching the stomach. The Rawl et al. 2014 case report (American Journal of Gastroenterology) describes a healthy adult who required endoscopic disimpaction. Practical prevention: always pre-soak chia (allow 5-10 minutes minimum), or consume dry chia in small amounts mixed with food (yogurt, oatmeal) where the existing food matrix prevents bolus impaction.
• Anticoagulant interaction — ALA modestly inhibits platelet aggregation. The effect is small individually but may compound with warfarin, dabigatran, rivaroxaban, apixaban, edoxaban, or with antiplatelet agents (aspirin, clopidogrel, ticagrelor). Most cardiologists consider chia at typical food doses (1-2 tablespoons daily) safe with these medications, but high-dose chia (3+ tablespoons daily) plus anticoagulation warrants conservatism and INR monitoring for warfarin patients.
• Pre-surgical use — discontinue chia at least 1 week before elective surgery if the daily intake is >2 tablespoons, because of the potential additive antiplatelet effect.
• Blood pressure with antihypertensive medication — the additive effect of chia with prescription antihypertensives (ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, thiazides) is generally clinically welcome but warrants home BP monitoring during initial weeks of high chia intake. Hypotension is the failure mode to watch for, particularly in elderly patients on multiple antihypertensives.
• Digestive tolerance — the high fiber load may cause bloating, gas, or constipation in fiber-naive individuals. Start with 1 teaspoon daily and titrate up over 2-4 weeks. Ensure adequate water intake (the soluble fiber requires water to function properly).
• Allergy — rare but documented; cross-reactivity with sesame is the most concerning allergy crossover. Anyone with sesame anaphylaxis should approach chia with medical supervision and an epinephrine auto-injector available for initial exposures.
• Diverticulitis caution — older guidance to avoid seeds in patients with diverticulosis has been largely retracted (Strate et al. 2008 JAMA showed no association between seed intake and diverticulitis), but during an active diverticulitis flare, low-residue diet remains standard and chia should be paused until resolution.

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Key Research Papers

1. de Lorgeril M et al. (1999). Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction (Lyon Diet Heart Study). Circulation. — PubMed (doi:10.1161/01.cir.99.6.779)
2. Estruch R et al. (2018). Primary Prevention of Cardiovascular Disease with a Mediterranean Diet (PREDIMED). NEJM. — PubMed (doi:10.1056/NEJMoa1800389)
3. Pan A et al. (2012). alpha-Linolenic acid and risk of cardiovascular disease: a systematic review and meta-analysis. American Journal of Clinical Nutrition. — PubMed (doi:10.3945/ajcn.112.044040)
4. Toscano LT et al. (2014). Chia flour supplementation reduces blood pressure in hypertensive subjects. Plant Foods for Human Nutrition. — PubMed (doi:10.1007/s11130-014-0408-y)
5. Vuksan V et al. (2007). Supplementation with the novel grain Salba improves major and emerging cardiovascular risk factors in type 2 diabetes. Diabetes Care. — PubMed (doi:10.2337/dc07-1144)
6. Burdge GC, Calder PC (2005). Conversion of alpha-linolenic acid to longer-chain polyunsaturated fatty acids in human adults. Reproduction Nutrition Development. — PubMed (doi:10.1051/rnd:2005047)
7. Brenna JT et al. (2009). alpha-Linolenic acid supplementation and conversion to n-3 long-chain polyunsaturated fatty acids. Prostaglandins Leukot Essent Fatty Acids. — PubMed (doi:10.1016/j.plefa.2009.01.004)
8. Mozaffarian D, Wu JHY (2011). Omega-3 fatty acids and cardiovascular disease. Journal of the American College of Cardiology. — PubMed (doi:10.1016/j.jacc.2011.06.063)
9. Nieman DC et al. (2009). Chia seed does not promote weight loss or alter disease risk factors in overweight adults. Nutrition Research. — PubMed (doi:10.1016/j.nutres.2009.04.004)
10. Tavares Luiz M et al. (2017). Effect of chia consumption on cardiovascular risk factors in humans: a systematic review. Nutrición Hospitalaria. — PubMed (doi:10.20960/nh.1287)
11. Rawl RM et al. (2014). Esophageal impaction by chia seeds. American Journal of Gastroenterology. — PubMed
12. Ayerza R Jr, Coates W (2005). Ground chia seed and chia oil effects on plasma lipids and fatty acids. Nutrition Research. — PubMed

PubMed Topic Searches

• PubMed: ALA cardiovascular disease
• PubMed: Chia seed blood pressure
• PubMed: ALA to EPA/DHA conversion
• PubMed: Omega-6 to omega-3 ratio
• PubMed: Lyon Diet Heart Study

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Connections

• Chia Seeds Overview
• Chia Seeds Benefits Hub
• Chia for Blood Sugar
• Chia for Calcium and Bone
• Chia for Hydration and Endurance
• Omega-3 Fatty Acids
• Flax Seeds (ALA)
• Walnuts (ALA)
• Salmon (EPA/DHA)
• Sardines (EPA/DHA)
• Cardiology
• Hypertension
• Atrial Fibrillation
• All Food
• Anti-Inflammatory Foods

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