Flaxseed oil contains a third, plant-based omega-3, alpha-linolenic acid (ALA). Other foods (especially walnuts) and oils (canola and soybean, for example) contain ALA. But at about 7 grams per tablespoon, flaxseed oil is by far the richest source.
The main problem with ALA is that to have the good effects attributed to omega-3s, it must be converted by a limited supply of enzymes into EPA and DHA. As a result, only a small fraction of it has omega-3's effects — 10%–15%, maybe less. The remaining 85%–90% gets burned up as energy or metabolized in other ways. So in terms of omega-3 "power," a tablespoon of flaxseed oil is worth about 700 milligrams (mg) of EPA and DHA. That's still more than the 300 mg of EPA and DHA in many 1-gram fish oil capsules, but far less than what the 7 grams listed on the label might imply.
https://www.health.harvard.edu/heart-health/why-not-flaxseed-oil
Omega 3 proven to kill cancer - vid
Omega-3 and omega-6 may play opposite roles in asthma
An NIEHS-funded study found that children with more dietary omega-3 fatty acids, present in foods such as salmon, had less severe asthma and fewer symptoms triggered by indoor air pollution. The same study showed an opposite effect for high levels of dietary omega-6 fatty acids, found in corn oil and other foods, which were linked to more severe asthma and more symptoms.
The researchers studied 135 children with asthma in Baltimore. Asthma severity and lung function were assessed at the beginning of the study, at three months, and at six months. At each time point, the researchers captured week-long average home indoor concentrations of air particulate matter, dietary intake of omega-3 and omega-6 fatty acids, and information on daily asthma symptoms and inhaler use.
The researchers found that for each additional gram of omega-6 in their reported diet, children had 29% higher odds of being in a more severe asthma category. With each 0.1-gram increase in omega-3 fatty acid intake, researchers saw 3-4% lower odds of daytime asthma symptoms. Overall, children who ate more omega-3 were less likely to have symptoms even at the same level of air pollution exposure.
According to the authors, the study suggests that the role of diet is important in understanding environmental exposures, and that children may be protected from some of the harmful effects of indoor air pollution if they eat more foods rich in omega-3 fatty acids and less foods rich in omega-6 fatty acids.
Citation: Brigham EP, Woo H, McCormack M, Rice J, Koehler K, Vulcain T, Wu T, Koch A, Sharma S, Kolahdooz F, Bose S, Hanson C, Romero K, Diette G, Hansel NN. 2019. Omega-3 and omega-6 intake modifies asthma severity and response to indoor air pollution in children. Am J Respir Crit Care Med; doi: 10.1164/rccm.201808-1474OC [Online 29 March 2019].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376635/
To determine the importance of genetic variability to fatty-acid biosynthesis, we studied FADS1 and FADS2, which encode rate-limiting enzymes for fatty-acid conversion. We performed genome-wide genotyping (n = 5,652 individuals) and targeted resequencing (n = 960 individuals) of the FADS region in five European population cohorts. We also analyzed available genomic data from human populations, archaic hominins, and more distant primates. Our results show that present-day humans have two common FADS haplotypes—defined by 28 closely linked SNPs across 38.9 kb—that differ dramatically in their ability to generate LC-PUFAs.
The more efficient, evolutionarily derived haplotype appeared after the lineage split leading to modern humans and Neanderthals and shows evidence of positive selection. This human-specific haplotype increases the efficiency of synthesizing essential long-chain fatty acids from precursors and thereby might have provided an advantage in environments with limited access to dietary LC-PUFAs. In the modern world, this haplotype has been associated with lifestyle-related diseases, such as coronary artery disease.
The δ-5 and δ-6 fatty-acid desaturases, which introduce double bonds after the fifth and sixth carbon atoms, respectively, from the carboxyl end of the carbon chain, are rate-limiting enzymes in the biosynthesis of omega-3 and omega-6 LC-PUFAs.5 These two key enzymes are encoded by FADS1 (MIM 606148) and FADS2 (MIM 606149), respectively, located in a head-to-head orientation on chromosome 11.
a single-nucleotide polymorphism is a germline substitution of a single nucleotide at a specific position in the genome.
The greater encephalization of modern humans might have required genetic adaptations of the fatty-acid metabolism to satisfy the high demand of LC-PUFAs needed to sustain the larger brain.19,20 In particular, mutations that increase the efficiency of converting the precursors ALA and LA to longer fatty acids are likely to be favored in environments with limited dietary access to these LC-PUFAs.
Our results show that in humans, two common and very distinct FADS haplotypes are strongly associated with LC-PUFA-synthesis levels. The haplotype associated with the enhanced ability to produce AA and DHA from their precursors is specific to humans and has appeared after the split of the common ancestor of humans and Neanderthals. This haplotype shows evidence of positive selection in African populations, in which it is presently almost fixed; the haplotype is less frequent outside Africa. We propose that the haplotype that provides a more efficient synthesis of LC-PUFAs might act as a thrifty genotype and represents a risk factor for lifestyle-related diseases, such as coronary artery disease.
The basic premise of the thrifty gene hypothesis is that certain populations may have genes that determine increased fat storage, which in times of famine represent a survival advantage, but in a modern environment result in obesity and type 2 diabetes.
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