Omega 3 Essential Fatty Acids (EFAs), particularly α-linolenic acid (ALA), are essential to health and vitality in humans. They are also nutrients that the body simply cannot synthesize itself and, therefore, must be obtained through one’s diet. As we age, our bodies tend to require additional EFAs to support various bodily functions such as heart and joint health. Therefore, supplementation or a doctor-recommended change in diet becomes a highly desirable course of action.
Chia Seed has been a staple in the diet of Central America for thousands of years. Chia contains large amounts of Omega 3 Fatty Acids, and is, in fact, among the most rich sources of EFAs derived from plants.
Our friends at the American Botanical Council recently posted an article about studies surrounding chia seeds and their effect on the levels of Omega 3 Fatty Acids in postmenopausal women. Here is that selection:
Milled Chia Seed Supplementation Improves Plasma Levels of Some Omega-3 Fatty Acids in Postmenopausal Women
Alpha-linolenic acid (ALA) is an n-3 polyunsaturated fatty acid that is converted to eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA) in humans. Humans cannot synthesize these essential polyunsaturated fatty acids de novo. Dietary sources of ALA include perilla (Perilla frutescens) seed, flax (Linum usitatissimum) seed, walnuts (Juglans spp.), and algae. The concern over increasing fish intake (another source of n-3 fatty acids) because of the heavy metals they contain and the sustainability of the harvest has heightened interest in these plant sources of n-3s. Chia (Salvia hispanica) seeds are also a good source of ALA and have recently become available in many food products (such as bread). The purpose of this open-label study was to evaluate the plasma response to EPA, DPA, and DHA after ingesting chia seeds in postmenopausal women.
Postmenopausal women (n = 10; aged 53-60 years) were recruited through local advertising in Kannapolis, North Carolina. Subject inclusion criteria included: being healthy without known disease; a body mass index (BMI) ≤ 35 kg/m2 and not currently on a weight reduction diet; no prior use of fish oil supplements or consuming ≥ 2 fish dishes/week; willingness to avoid all forms of fish oil and flaxseed oil supplements; limiting fish and seafood intake to ≤ 1x/week; and restricting intake of plant oils rich in n-6 fatty acids, such as sunflower (Helianthus annuus), safflower (Carthamus tinctorius), soybean (Glycine max), corn (Zea mays), and similar plant oils. Subjects were instructed to use moderate amounts of olive (Olea europaea) oil and canola oil (from rape [Brassica napus] seed) during the study and to follow their normal diet and exercise routines. Subjects consumed 25 g/day of milled chia seeds (containing 16.4 g/100 g of ALA) (Chia Farms, Inc.; Orlando, Florida) for 7 weeks by sprinkling the seed packets into fruit juices, yogurt, breakfast cereal, salads, and other dishes at 1 meal or spread throughout the day. Compliance was monitored by counting the empty supplement packets. Fasting blood was drawn at baseline and at 1, 2, 3, 5, and 7 weeks. Subjects recorded a food and symptom log at baseline, 3 weeks, and 7 weeks.
According to the food diaries, dietary intake of fat, ALA, EPA, DPA, and DHA did not change over the course of the study. Symptoms of digestive health, hunger, energy level, illness, pain, allergies, stress, focus/concentration, and overall well-being as assessed by the subject symptom logs did not differ significantly between baseline and 7 weeks. BMI did not change over the course of the study.
Plasma ALA significantly increased with chia consumption over time (P < 0.001), with a 138% increase in ALA from baseline to the average of weeks 5 and 7. ALA was also significantly increased after chia consumption compared with baseline at week 1, 2, and 3 (P < 0.0125 for all). After chia consumption, plasma EPA significantly increased over time by 30% above baseline levels (P = 0.019), with significant elevations at week 1 and the average of weeks 5 and 7 (P < 0.0125 for all). Individual plots for ALA and EPA indicated large inter-individual variations both pre-study and in response to chia seed supplementation. There was a significant positive correlation between plasma EPA and ALA during chia seed supplementation across all time points (r = 0.84, P = 0.02). Chia supplementation had no significant effect on DPA or DHA levels.
The authors conclude that 25 g/day of milled chia seeds for 7 weeks significantly increased plasma ALA and EPA, but not DPA and DHA, in postmenopausal women. They do also note that it is unclear what the health implications of this increase might be. However, this amount is too high a level of chia seeds because this is 8 g of oil and 5.6 g of ALA, a number that is above the European Union (EU) suggested maximum consumption of 5 g of ALA/day. It has been suggested that an optimal dose is 3 g/day. Twenty-five g of chia seeds are also over 160 calories of fat. It should be noted that there are products on the market with defatted chia seed meal. It would be interesting to compare these products to the product used in this study at an appropriate dosage. Based on these results compared with previous studies, the authors conclude that the ALA from milled chia seeds more readily enters the plasma than whole seeds. It is unclear why the authors limited the study to postmenopausal women.
The levels of ALA and EPA peaked at 5 weeks, and then declined at 7 weeks. The study ended at 7 weeks. The study findings are limited by the duration of treatment and the population sample size. It is unknown what happens to the ALA and EPA levels beyond 7 weeks. Do the levels continue to decline or can the decline be attributed to the small study size, particularly since there were high inter-individual differences? This study should be viewed as a pilot study and should be repeated with a larger population and for a longer duration.
—Heather S. Oliff, PhD
