Chia (Salvia hispanica) and Cardiovascular / heart health: evidence and sources

Chia ( Salvia hispanica L.) is an annual herbaceous plant, originally from southern Mexico and northern Guatemala - nowadays grown all over the world. In recent years, there has been an increase in demand for plant foods with health-promoting properties, and chia is a main actor in this process due to its high nutritional and functional value and its chemical composition rich in PUFAs, mainly ω-3, as well as protein, dietary fiber, and bioactive compounds. Chia has been explored in different research models for health and the prevention of human diseases. Evidence has suggested potential for improving insulin resistance, disordered lipid profiles, glucose tolerance and even adiposity. The aim of this study was to evaluate the effect of consumption of chia seeds on the lipid profile, triglycerides, and serum ω-3 fatty acids in adults. This systematic review included all randomized controlled trials (parallel or crossover design) published up to August 2020 in the main databases Medline, Embase, Scopus, Web of Science, and Scielo. Two independent authors selected and extracted data from those articles. After the selection process, 10 clinical trials were included. Forest plots and summary tables were constructed to present data and sensitivity subgroup analyses were performed for some of the outcomes. The results showed that chia consumption suggests a protective effect on the lipid profile, decreasing TC (MD = -2.98, 95% CI = [-9.98; 4.02]), TG (MD = -14.09 mg dL -1 , 95% CI = [-33.46; 5.28]), and LDL (MD = 2.07 mg dL -1 ; 95% CI = [-5.05; 9.19]) and increasing HDL (MD = -2.92 mg dL -1 , 95% CI = [-5.91; 0.06]). Regarding serum fatty acids, chia reduced FFA and SFA and increased PUFAs, ALA, EPA, and LA. It has also reduced DHA while not changing DPA. The intake of chia appears to have a neutral or beneficial effect on some markers of the lipid and fatty acid profile.

Context Chia seed is a popular dietary supplement, taken mainly for its high content of alpha-linolenic acid, vegetable protein, and dietary fiber, yet information about its clinical effects is lacking. Objective This review aims to summarize the clinical evidence regarding the use of chia seed for a wide variety of health conditions. Data sources A number of databases, including PubMed and Embase, were searched systematically. Study selection Randomized controlled trials that assessed the clinical effects of chia seed consumption in human participants were included. The quality of trials was assessed using the Cochrane Risk of Bias Tool. Data extraction Data on study design, blinding status, characteristics of participants, chia seed intervention, comparator, clinical assessment, duration of intake, interval of assessment, and study funding status were extracted. Meta-analysis was performed. Results Twelve trials were included. Participants included healthy persons, athletes, diabetic patients, and individuals with metabolic syndrome. Pooling of results showed no significant differences except for the following findings of subgroup analysis at higher doses of chia seed: (1) lower postprandial blood glucose level (mean difference [MD] of -33.95 incremental area under the curve [iAUC] [mmol/L × 2 h] [95%CI, -61.85, -6.05] and -51.60 iAUC [mmol/L × 2 h] [95%CI, -79.64, -23.56] at medium doses and high doses, respectively); (2) lower high-density lipoprotein in serum (MD of -0.10 mmol/L [95%CI, -0.20, -0.01]); and (3) lower diastolic blood pressure (MD of -7.14 mmHg [95%CI, -11.08, -3.19]). The quality of all evidence assessed using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach was low or very low. All trials employed only surrogate markers as outcomes. Conclusions Future trials with improved methodological quality, well-described clinical events, and validated surrogate markers as outcomes are needed to support the potential health benefits of chia seed consumption. Systematic review registration PROSPERO registration no. CRD42015029990.

Introduction chia is a seed rich in such nutrients as proteins, n-3 fatty acids and especially alpha-linolenic acid (ALA), minerals, fibers and antioxidants. Efforts have been made to assess whether human consumption of chia can reduce cardiovascular risk factors; however, it has not been established as effective and the findings of the few studies to have looked into the matter are inconsistent. Aim to systematize the findings of studies assessing the effect the consumption of chia seed, either milled or whole, has in the prevention/control of cardiovascular risk factors in humans. Methods this is a systematic literature review (SLR) with no meta-analysis. The articles scrutinizedwere identified in the electronic databases Lilacs, Medline (Pub- Med version), Cochrane, Scielo, Scopus, and Web of Science under the keywords"dyslipidemia" or "dislipidemia", "hyperlipidemia" or "hiperlipidemia", "obesity" or "obesidade", "salvia"or"salviahispanica", "Lamiaceae" or "chia", "hypertension" or "hipertensão", "hypertrygliceridemia" or "hipertrigliceridemia", and "riscocardiovascular" or "cardiovascularrisk." We chose for our selection English-, Portuguese- or Spanish-language articles about clinical trials on humans and published within the last ten years. The biases of risk analysis were carried out considering 6 of the 8 criteria of the Cochrane Handbook for Systematic Reviews of Interventions Version 5.1. Findings seven studies (n = 200) fit our inclusion criteria. Of the chosen clinical trials, only one was not randomized. Five of the studies were blind experiments. Two of the studies were acute trials, both of them randomized. Of the chia seed interventions, one study showed a significant drop in systolic blood pressure (SBP) and inflammatory markers, yet there was no change in body mass, lipid profile or blood sugar. In four of the studies reviewed there was a significant spike in ALA and eicosapentaenoic acid (EPA), with no significant change to other parameters. In the acute trials, post-prandial blood sugar was significantly lower. Only one study showed a significant drop in triglycerides (TG), body mass and inflammatory markers; however, the chia seed in that case was mixed with other foods. Most of the studies showed unclear or low risk of bias. Two studies showed a high risk of bias because not all the pre-specified primary outcomes were reported in the findings. Conclusion most of the studies did not demonstrate statistically significant results in relation to cardiovascular disease (CVD) risk factors. The evidence regarding the relationship between chia seed consumption and cardiovascular risk factors are insufficient, and the studies included in this review present numerous limitations. Further research is hence needed.

Despite strong correlations linking whole-grain consumption to reductions in heart disease, the physiological mechanisms involved remain ambiguous. We assessed whether Salba (Salvia Hispanica L.) whole grain reduces postprandial glycemia in healthy subjects, as a possible explanation for its cardioprotective effects observed in individuals with diabetes. The study used acute, randomized, double-blind, controlled design in which 11 healthy individuals (6 males and 5 females; body mass index 22.3+/-2.8 kg/m(2)) received 0, 7, 15 or 24 g of Salba baked into white bread. Capillary samples and appetite ratings were collected over 2 h after consumption. A dose-response reduction in postprandial glycemia (P=0.002, r(2)=0.203) was observed with all three doses of Salba, significantly decreasing incremental areas under the curve (iAUCs) and time point-specific blood glucose (P<0.05). Appetite ratings were decreased at 60 min after high, 90 min after high and intermediate and at 120 min after all treatments (P<0.05). Decrease in postprandial glycemia provides a potential explanation for improvements in blood pressure, coagulation and inflammatory markers previously observed after 12-week Salba supplementation in type II diabetes.

Background The effect of increasing the intake of dietary fiber on glycemic control in patients with type 2 diabetes mellitus is controversial. Methods In a randomized, crossover study, we assigned 13 patients with type 2 diabetes mellitus to follow two diets, each for six weeks: a diet containing moderate amounts of fiber (total, 24 g; 8 g of soluble fiber and 16 g of insoluble fiber), as recommended by the American Diabetes Association (ADA), and a high-fiber diet (total, 50 g; 25 g of soluble fiber and 25 g of insoluble fiber), containing foods not fortified with fiber (unfortified foods). Both diets, prepared in a research kitchen, had the same macronutrient and energy content. We compared the effects of the two diets on glycemic control and plasma lipid concentrations. Results Compliance with the diets was excellent. During the sixth week, the high-fiber diet, as compared with the the sixth week of the ADA diet, mean daily preprandial plasma glucose concentrations were 13 mg per deciliter [0.7 mmol per liter] lower (95 percent confidence interval, 1 to 24 mg per deciliter [0.1 to 1.3 mmol per liter]; P=0.04) and mean median difference, daily urinary glucose excretion 1.3 g (0.23; 95 percent confidence interval, 0.03 to 1.83 g; P= 0.008). The high-fiber diet also lowered the area under the curve for 24-hour plasma glucose and insulin concentrations, which were measured every two hours, by 10 percent (P=0.02) and 12 percent (P=0.05), respectively. The high-fiber diet reduced plasma total cholesterol concentrations by 6.7 percent (P=0.02), triglyceride concentrations by 10.2 percent (P=0.02), and very-low-density lipoprotein cholesterol concentrations by 12.5 percent (P=0.01). Conclusions A high intake of dietary fiber, particularly of the soluble type, above the level recommended by the ADA, improves glycemic control, decreases hyperinsulinemia, and lowers plasma lipid concentrations in patients with type 2 diabetes.

The purposes of the present study were to analyze liver inflammation and endothelial dysfunction in an experimental model of metabolic syndrome (MS) induced by chronic administration of a sucrose-rich diet (SRD) and to evaluate the effects of chia seed as a therapeutic strategy. Male Wistar rats were fed with a reference diet (RD) for 6 months or a SRD for 3 months. Then, the latter group was randomly divided into two subgroups. One subgroup continued receiving the SRD for up to 6 months and the other was fed with a SRD where whole chia seed was incorporated as a source of dietary fat for the next 3 months (SRD + CHIA). Results showed that rats fed a SRD for a long period of time developed dyslipidemia, hyperglycemia, inflammation and endothelial dysfunction. Hepatic NAS, IL-1β, NFκB p65, PAI-1, and F4-80 expression, as well as MPO activity were significantly increased and IL-10 expression was significantly decreased; this was accompanied by increased plasma IL-6 and TNF-α levels in rats fed a SRD. In addition, serum and liver nitric oxide (NO) levels and nitric oxide synthase (NOS) were significantly increased in the SRD group. In addition, a significant increase in hepatic iNOS expression and a positive correlation of this with liver NFκB p65 was found. We observed a significant increase in hepatic intercellular adhesion molecule (ICAM), and a negative correlation of this with liver Nrf2 was found. The administration of chia seed for 3 months reversed dyslipidemia, hyperglycemia, inflammation and endothelial dysfunction. In the liver tissue, NAS, IL-1β, IL-10, NFκB p65, PAI-1, and F4-80 expression and MPO activity were normalized. Serum and liver NO and NOS levels and hepatic iNOS expression were decreased and this last one was associated with a decrease in liver NFκB p65 levels. Hepatic ICAM-1 was normalized and negatively correlated with liver NrF2 levels. This study showed new aspects of liver inflammation and endothelial dysfunction in dyslipidemic insulin resistant rats chronically fed with a sucrose-rich diet. In addition, we demonstrated new properties and molecular mechanisms associated with beneficial effects on inflammation and endothelial dysfunction of chia seed as a therapeutic strategy.