-
The Canadian Journal of Cardiology Nov 2010Preventing the occurrence of cardiovascular disease (CVD) with nutritional interventions is a therapeutic strategy that may warrant greater research attention. The... (Review)
Review
Preventing the occurrence of cardiovascular disease (CVD) with nutritional interventions is a therapeutic strategy that may warrant greater research attention. The increased use of omega (ω)-3 fatty acids is a powerful example of one such nutritional strategy that may produce significant cardiovascular benefits. Marine food products have provided the traditional dietary sources of ω-3 fatty acids. Flaxseed is an alternative to marine products. It is one of the richest sources of the plant-based ω-3 fatty acid, alpha-linolenic acid (ALA). Based on the results of clinical trials, epidemiological investigations and experimental studies, ingestion of ALA has been suggested to have a positive impact on CVD. Because of its high ALA content, the use of flaxseed has been advocated to combat CVD. The purpose of the present review was to identify the known cardiovascular effects of flaxseed and ALA and, just as importantly, what is presently unknown.
Topics: Cardiovascular Diseases; Clinical Trials as Topic; Evidence-Based Medicine; Flax; Humans; Phytotherapy; Seeds; Treatment Outcome; alpha-Linolenic Acid
PubMed: 21076723
DOI: 10.1016/s0828-282x(10)70455-4 -
Asia Pacific Journal of Clinical... Jun 2017Omega-3 fatty acid intake during pregnancy has been confirmed to affect newborn birth outcomes in the developed world. However, the association between maternal omega-3...
BACKGROUND
Omega-3 fatty acid intake during pregnancy has been confirmed to affect newborn birth outcomes in the developed world. However, the association between maternal omega-3 fatty acid intake and birth size is unknown in developing countries.
OBJECTIVE
To examine the association of maternal omega-3 fatty acid intake with newborn birth size.
METHODS AND STUDY DESIGN
A cross-sectional study was conducted, involving 282 pregnant women aged 19-40 years who had a gestational age of >32 weeks and received antenatal care at 10 health centres and one referral hospital in East Jakarta, Indonesia. Maternal habitual intake of omega-3 fatty acids, including α-linolenic acid, docosahexaenoic acid, and eicosapentaenoic acid, was assessed using a semiquantitative food frequency questionnaire. Birth weight and head circumference were measured using a paediatric weighing scale and tape, respectively, and birth length was obtained from medical records. Multiple linear regression analysis was performed to provide adjusted associations.
RESULTS
The median total intake of omega-3 fatty acids, docosahexaenoic acid, eicosapentaenoic acid, and α-linolenic acid was lower than the recommended dietary intake. The newborns of mothers with an α-linolenic acid intake lower than 0.82 g/d had a significantly lower (β=114, 95% confidence interval=-216, -13.5; p=0.014) weight compared with those of mothers with high α-linolenic acid intake, after adjustment for confounding factors.
CONCLUSION
Inadequate maternal intake of α-linolenic acid, but not omega-3 fatty acids, docosahexaenoic acid, or eicosapentaenoic acid, was associated with lower birth weight. Enhanced promotion of consumption of foods rich in essential fatty acids during pregnancy may facilitate attaining optimal infant weight in urban areas.
Topics: Adult; Birth Weight; Cohort Studies; Diet; Female; Humans; Indonesia; Infant, Newborn; Pregnancy; Prenatal Nutritional Physiological Phenomena; Urban Population; Young Adult; alpha-Linolenic Acid
PubMed: 28625031
DOI: 10.6133/apjcn.062017.s1 -
International Journal of Molecular... Apr 2024The plant-derived α-linolenic acid (ALA) is an essential n-3 acid highly susceptible to oxidation, present in oils of flaxseeds, walnuts, canola, perilla, soy, and... (Review)
Review
The plant-derived α-linolenic acid (ALA) is an essential n-3 acid highly susceptible to oxidation, present in oils of flaxseeds, walnuts, canola, perilla, soy, and chia. After ingestion, it can be incorporated in to body lipid pools (particularly triglycerides and phospholipid membranes), and then endogenously metabolized through desaturation, elongation, and peroxisome oxidation to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), with a very limited efficiency (particularly for DHA), beta-oxidized as an energy source, or directly metabolized to C18-oxilipins. At this moment, data in the literature about the effects of ALA supplementation on metabolic syndrome (MetS) in humans are inconsistent, indicating no effects or some positive effects on all MetS components (abdominal obesity, dyslipidemia, impaired insulin sensitivity and glucoregulation, blood pressure, and liver steatosis). The major effects of ALA on MetS seem to be through its conversion to more potent EPA and DHA, the impact on the n-3/n-6 ratio, and the consecutive effects on the formation of oxylipins and endocannabinoids, inflammation, insulin sensitivity, and insulin secretion, as well as adipocyte and hepatocytes function. It is important to distinguish the direct effects of ALA from the effects of EPA and DHA metabolites. This review summarizes the most recent findings on this topic and discusses the possible mechanisms.
Topics: Metabolic Syndrome; Humans; alpha-Linolenic Acid; Animals; Fatty Acids, Unsaturated; Dietary Supplements; Insulin Resistance
PubMed: 38732139
DOI: 10.3390/ijms25094909 -
Current Opinion in Clinical Nutrition... Mar 2002Alpha-linolenic acid (18:3n-3) is the major n-3 (omega 3) fatty acid in the human diet. It is derived mainly from terrestrial plant consumption and it has long been... (Review)
Review
Alpha-linolenic acid (18:3n-3) is the major n-3 (omega 3) fatty acid in the human diet. It is derived mainly from terrestrial plant consumption and it has long been thought that its major biochemical role is as the principal precursor for long chain polyunsaturated fatty acids, of which eicosapentaenoic (20:5n-3) and docosahexaenoic acid (22:6n-3) are the most prevalent. For infants, n-3 long chain polyunsaturated fatty acids are required for rapid growth of neural tissue in the perinatal period and a nutritional supply is particularly important for development of premature infants. For adults, n-3 long chain polyunsaturated fatty acid supplementation is implicated in improving a wide range of clinical pathologies involving cardiac, kidney, and neural tissues. Studies generally agree that whole body conversion of 18:3n-3 to 22:6n-3 is below 5% in humans, and depends on the concentration of n-6 fatty acids and long chain polyunsaturated fatty acids in the diet. Complete oxidation of dietary 18:3n-3 to CO2 accounts for about 25% of 18:3n-3 in the first 24 h, reaching 60% by 7 days. Much of the remaining 18:3n-3 serves as a source of acetate for synthesis of saturates and monounsaturates, with very little stored as 18:3n-3. In term and preterm infants, studies show wide variability in the plasma kinetics of 13C n-3 long chain polyunsaturated fatty acids after 13C-18:3n-3 dosing, suggesting wide variability among human infants in the development of biosynthetic capability to convert 18:3n-3 to 22:6n3. Tracer studies show that humans of all ages can perform the conversion of 18:3n-3 to 22:6n3. Further studies are required to establish quantitatively the partitioning of dietary 18:3n-3 among metabolic pathways and the influence of other dietary components and of physiological states on these processes.
Topics: Energy Metabolism; Fatty Acids, Omega-3; Fatty Acids, Omega-6; Fatty Acids, Unsaturated; Humans; Oxidation-Reduction; alpha-Linolenic Acid
PubMed: 11844977
DOI: 10.1097/00075197-200203000-00002 -
Progress in Lipid Research Nov 2009There is little doubt regarding the essential nature of alpha-linolenic acid (ALA), yet the capacity of dietary ALA to maintain adequate tissue levels of long chain n-3... (Review)
Review
There is little doubt regarding the essential nature of alpha-linolenic acid (ALA), yet the capacity of dietary ALA to maintain adequate tissue levels of long chain n-3 fatty acids remains quite controversial. This simple point remains highly debated despite evidence that removal of dietary ALA promotes n-3 fatty acid inadequacy, including that of docosahexaenoic acid (DHA), and that many experiments demonstrate that dietary inclusion of ALA raises n-3 tissue fatty acid content, including DHA. Herein we propose, based upon our previous work and that of others, that ALA is elongated and desaturated in a tissue-dependent manner. One important concept is to recognize that ALA, like many other fatty acids, rapidly undergoes beta-oxidation and that the carbons are conserved and reused for synthesis of other products including cholesterol and fatty acids. This process and the differences between utilization of dietary DHA or liver-derived DHA as compared to ALA have led to the dogma that ALA is not a useful fatty acid for maintaining tissue long chain n-3 fatty acids, including DHA. Herein, we propose that indeed dietary ALA is a crucial dietary source of n-3 fatty acids and its dietary inclusion is critical for maintaining tissue long chain n-3 levels.
Topics: Brain; Cardiovascular System; Diet; Dietary Supplements; Docosahexaenoic Acids; Fatty Acids, Omega-3; Humans; Public Health; alpha-Linolenic Acid
PubMed: 19619583
DOI: 10.1016/j.plipres.2009.07.002 -
Molecular Nutrition & Food Research Feb 2022Nutrients stimulate the secretion of glucagon-like peptide-1 (GLP-1), an incretin hormone, secreted from enteroendocrine L-cells which decreases food intake. Thus, GLP-1...
SCOPE
Nutrients stimulate the secretion of glucagon-like peptide-1 (GLP-1), an incretin hormone, secreted from enteroendocrine L-cells which decreases food intake. Thus, GLP-1 analogs are approved for the treatment of obesity, yet cost and side effects limit their use. L-cells are mainly localized in the distal ileum and colon, which hinders the utilization of nutrients targeting GLP-1 secretion. This study proposes a controlled delivery system for nutrients, inducing a prolonged endogenous GLP-1 release which results in a decrease food intake.
METHODS AND RESULTS
α-Linolenic acid (αLA) was loaded into thermally hydrocarbonized porous silicon (THCPSi) particles. In vitro characterization and in vivo effects of αLA loaded particles on GLP-1 secretion and food intake were studied in mice. A total of 40.4 ± 3.2% of loaded αLA is released from particles into biorelevant buffer over 24 h, and αLA loaded THCPSi significantly increased in vitro GLP-1 secretion. Single-dose orally given αLA loaded mesoporous particles increased plasma active GLP-1 levels at 3 and 4 h and significantly reduced the area under the curve of 24 h food intake in mice.
CONCLUSIONS
αLA loaded THCPSi particles could be used to endogenously stimulate sustain gastrointestinal hormone release and reduce food intake.
Topics: Animals; Colon; Eating; Glucagon-Like Peptide 1; Mice; Nutrients; alpha-Linolenic Acid
PubMed: 34882959
DOI: 10.1002/mnfr.202100978 -
Plant Physiology and Biochemistry : PPB Oct 2014Using an in vitro system composed of crushed leaf tissues to simulate the wounding response in rice leaves, we established that synthesis of jasmonic acid (JA) and...
Using an in vitro system composed of crushed leaf tissues to simulate the wounding response in rice leaves, we established that synthesis of jasmonic acid (JA) and jasmonic acid-isoleucine (JA-Ile) can only occur in unwounded tissue and, in wounded tissue, that only the chloroplast-located section of the octadecanoid pathway is active, resulting in the accumulation of 12-oxo-phytodienoic acid (OPDA). We further showed that OPDA accumulation in vitro was inhibited by 90% using the general lipase inhibitor, tetrahydrolipstatin, indicating that production of α-linolenic acid was the rate-limiting step in octadecanoid pathway activity in rice following wounding and the enzyme capacity for an active pathway was already present. We confirmed this result by showing that added α-linolenic acid stimulated OPDA synthesis in vitro and stimulated OPDA, JA and JA-Ile synthesis in vivo in unwounded tissue. Thus, the response to wounding can be mimicked by the provision of free α-linolenic acid. Our results draw attention to the key importance of lipase activity in initiation of JA and JA-Ile biosynthesis and our lack of knowledge of the cognate lipase(s), lipase substrate identity and mechanism(s) of activation in wounded and unwounded tissue.
Topics: Oryza; Oxylipins; Plant Leaves; alpha-Linolenic Acid
PubMed: 25129550
DOI: 10.1016/j.plaphy.2014.07.013 -
Circulation Jul 2008Intake of long-chain n-3 fatty acids found in fish is low in many countries worldwide. alpha-Linolenic acid could be a viable cardioprotective alternative to these fatty...
BACKGROUND
Intake of long-chain n-3 fatty acids found in fish is low in many countries worldwide. alpha-Linolenic acid could be a viable cardioprotective alternative to these fatty acids in these countries.
METHODS AND RESULTS
Cases (n=1819) with a first nonfatal acute myocardial infarction and population-based controls (n=1819) living in Costa Rica matched for age, sex, and area of residence were studied. Fatty acids were assessed by gas chromatography in adipose tissue samples and by a validated food frequency questionnaire specifically designed for this population. Odds ratios and 95% confidence intervals were calculated from multivariate conditional logistic regression models. alpha-Linolenic acid in adipose tissue ranged from 0.36% in the lowest decile to 1.04% in the highest decile. The corresponding median levels of intake were 0.42% and 0.86% energy. Greater alpha-linolenic acid (assessed either in adipose or by questionnaire) was associated with lower risk of myocardial infarction. The odds ratios for nonfatal myocardial infarction for the highest compared with the lowest deciles were 0.41 (95% confidence interval, 0.25 to 0.67) for alpha-linolenic acid in adipose tissue and 0.61 (95% confidence interval, 0.42 to 0.88) for dietary alpha-linolenic acid. The relationship between alpha-linolenic acid and myocardial infarction was nonlinear; risk did not decrease with intakes > approximately 0.65% energy (1.79 g/d). Fish or eicosapentaenoic acid and docosahexaenoic acid intake at the levels found in this population did not modify the observed association.
CONCLUSIONS
Consumption of vegetable oils rich in alpha-linolenic acid could confer important cardiovascular protection. The apparent protective effect of alpha-linolenic acid is most evident among subjects with low intakes.
Topics: Adipose Tissue; Aged; Chromatography, Gas; Costa Rica; Fatty Acids; Female; Humans; Male; Middle Aged; Myocardial Infarction; Plant Oils; Risk; alpha-Linolenic Acid
PubMed: 18606916
DOI: 10.1161/CIRCULATIONAHA.107.762419 -
The British Journal of Nutrition Jun 2016Description of α-linolenic acid (cis-9,cis-12,cis-15-18 : 3, ALA) metabolism in the rumen is incomplete. Ruminal digesta samples were incubated with ALA and buffer...
Description of α-linolenic acid (cis-9,cis-12,cis-15-18 : 3, ALA) metabolism in the rumen is incomplete. Ruminal digesta samples were incubated with ALA and buffer containing water or deuterium oxide to investigate the products and mechanisms of ALA biohydrogenation. Geometric Δ9,11,15-18 : 3 isomers were the main intermediates formed from ALA. An increase in the n+1 isotopomers of Δ9,11,15-18 : 3 was due to 2H labelling at C-13. Isomers of Δ9,11,13-18 : 3, cis-7,cis-12,cis-15-18 : 3 and cis-8,cis-12,cis-15-18 : 3 were also formed. No increase in n+1 isotopomers of Δ7,12,15-18 : 3 or Δ8,12,15-18 : 3 was detected. Enrichment in n+2 isotopomers of 18 : 2 products indicated that ALA metabolism continued via the reduction of 18 : 3 intermediates. Isomers of Δ9,11,15-18 : 3 were reduced to Δ11,15-18 : 2 labelled at C-9 and C-13. ALA resulted in the formation of Δ11,13-18 : 2 and Δ12,14-18 : 2 containing multiple 2H labels. Enrichment of the n+3 isotopomer of Δ12,15-18 : 2 was also detected. Metabolism of ALA during incubations with rumen contents occurs by one of three distinct pathways. Formation of Δ9,11,15-18 : 3 appears to be initiated by H abstraction on C-13. Octadecatrienoic intermediates containing cis-12 and cis-15 double bonds are formed without an apparent H exchange with water. Labelling of Δ9,11,13-18 : 3 was inconclusive, suggesting formation by an alternative mechanism. These findings explain the appearance of several bioactive fatty acids in muscle and milk that influence the nutritional value of ruminant-derived foods.
Topics: Animals; Cattle; Dietary Fats; Digestion; Female; Hydrogenation; Isomerism; Linoleic Acids, Conjugated; Meat; Milk; Muscles; Rumen; Ruminants; alpha-Linolenic Acid
PubMed: 27087357
DOI: 10.1017/S0007114516001446 -
Biochimica Et Biophysica Acta Sep 1994Cholesterol is demonstrated to condense phosphatidylcholine (PC) monolayers and bilayers containing stearic acid in the sn-1 position and alpha-linolenic acid in the... (Comparative Study)
Comparative Study
Cholesterol is demonstrated to condense phosphatidylcholine (PC) monolayers and bilayers containing stearic acid in the sn-1 position and alpha-linolenic acid in the sn-2 position (18:0, alpha-18:3 PC) but has no effect when gamma-linolenic acid occupies the sn-2 position (18:0,gamma-18:3 PC). Cholesterol-induced condensation is measured by area/molecule determinations made on monolayers using a Langmuir trough, while condensation in bilayers is followed by the fluorescent dyes merocyanine (MC540) and dansyllysine. Permeability to erythritol is also demonstrated to be diminished by cholesterol for the condensable 18:0,alpha-18:3 PC bilayer membranes but not the 18:0,gamma-18:3 PC membranes. alpha- and gamma-linolenic acid are isomers containing 18 carbons and three unsaturations. Both fatty acids have unsaturations at positions 9 and 12 and differ only in the location of the third unsaturation, at either position 6 for gamma-linolenic acid (an omega-6 fatty acid) and at position 15 for alpha-linolenic acid (an omega-3 fatty acid). Here lipid-cholesterol interaction is used to distinguish the effect of position of unsaturation on membrane structure.
Topics: Cholesterol; Isomerism; Lipid Bilayers; Phosphatidylcholines; alpha-Linolenic Acid; gamma-Linolenic Acid
PubMed: 7918592
DOI: 10.1016/0005-2760(94)90036-1