17 Science-Based Benefits of Omega-3 Fatty Acids
Omega-3 fatty acids are incredibly important for your body and brain. Inflammation: Omega-3s reduce the production of some substances released that omega-3 supplements can reduce the symptoms of ADHD. Studies have consistently observed a connection between higher omega-3 intake and. Thus, the fatty acid composition of cells involved in the inflammatory response Fatty Acid Composition of Cells Involved in Inflammation and its Modification by Marine n-3 Fatty Acids . EPA and DHA also give rise to resolvins and related compounds (e.g., Add to FavoritesView more options. This article focuses on the role of omega-3 fatty acids as precursors for lipid . especially when considered in relation to omega-6 fatty acids (Kris-Etherton et al. . those metabolized by the LOX (5-LOX and 12/LOX) enzymes were added.
Mechanisms by which Polyunsaturated Fatty Acids can Influence Inflammatory Cell Function PUFAs can influence inflammatory cell function, and so inflammatory processes, by a variety of mechanisms as follows: Membrane phospholipids are substrates for the generation of second messengers like diacylglycerol and it has been demonstrated that the fatty acid composition of such second messengers, which is determined by that of the precursor phospholipid, can influence their activity [ 27 ].
In addition, membrane phospholipids are substrates for the release of non-esterfied PUFAs intracellularly — the released PUFAs can act as signaling molecules, ligands or precursors of ligands for transcription factors, or precursors for biosynthesis of lipid mediators which are involved in regulation of many cell and tissue responses, including aspects of inflammation and immunity see below.
Thus, changes in membrane phospholipid fatty acid composition, as described above, can influence the function of cells involved in inflammation via: The multitude of potential mechanisms involved and their complexity has made it difficult to fully understand the actions of PUFAs within inflammatory processes.
The Benefits of Omega-3 Fatty Acids for Arthritis
This difficulty has been further compounded by the variety of experimental approaches that have been used, including the method of presentation of PUFAs of interest to inflammatory cells in order to study their effects.
For example, many in vitro studies have exposed cells to non-esterified fatty acids, often at concentrations that might not be achieved physiologically. Thus, effects of non-esterified PUFAs on responses of lymphocytes [ 2 ], monocytes [ 28 ], macrophages [ 82930313233 ], neutrophils [ 343536 ] and endothelial cells [ 373839 ] have been demonstrated. Physiologically, the concentration of non-esterified n-3 PUFAs and also arachidonic acid is quite low.
These fatty acids are carried in the bloodstream at much higher concentrations in more complex lipids triglycerides, phospholipds, cholesteryl esters within lipoproteins. Many of the cell types involved in inflammatory responses express lipoprotein receptors e. Thus, lipoproteins may affect inflammatory cell function [ 4344 ], perhaps due to their component fatty acids. Inflammatory cells may also access fatty acids from lipoproteins by hydrolysing them extracellularly as has been demonstrated for macrophages [ 45 ] and lymphocytes [ 46 ].
Thus, cells involved in inflammatory processes are exposed to fatty acids, including PUFAs, in many different forms, and they may access fatty acids from their environment by a variety of mechanisms.
The effect of the form of presentation of PUFAs to inflammatory cells can be examined in the cell culture setting and studies to date indicate that non-esterified fatty acids [ 282930313233343536373839 ], complex lipids like triglycerides [ 46 ], intact lipoproteins [ 44 ], and oxidized forms of fatty acids and other lipids [ 404142 ] all influence inflammatory cell responses, frequently with different effects or different potencies of n-6 and n-3 PUFAs.
Following increased dietary intake of marine n-3 PUFAs their concentrations increase in complex lipids within the bloodstream triglycerides, phospholipids, cholesteryl estersas well as within the membrane phospholipids of cells and tissues including those involved in inflammatory responses see aboveand there is a small increase in their concentration within the circulating non-esterfied fatty acid pool; the latter increase is small because circulating non-esterfied fatty acids derive principally from adipose tissue triglyceride breakdown and adipose tissue triglycerides contain very little EPA and DHA.
Thus, following increased intake of EPA and DHA, both the cells involved in inflammation and their extracellular environment e. Many studies have examined the effect of increased intake of marine n-3 PUFAs on the function of cells typically involved in inflammation taken from the bloodstream neutrophils, eosinophils, monocytes, lymphocytes or, in the case of animal studies tissues and subsequently cultured.
In many, probably most, cases the in vivo situation is not maintained during the ex vivo culture period, in that the n-3 PUFA enriched cells are maintained in an environment that is different from that to which they were exposed in vivo i. Thus, the in vivo situation is not replicated in the ex vivo setting. This hampers the full interpretation of the findings of such research. Biosynthesis, Roles in Inflammation, and the Impact of Marine n-3 fatty acids 4.
Eicosanoids Generated from Arachidonic Acid Eicosanoids are key mediators and regulators of inflammation and immunity and are generated from 20 carbon PUFAs. Eicosanoids, which include PGs, thromboxanes, LTs and other oxidised derivatives, are generated from arachidonic acid by the metabolic processes summarized in Figure 2. Eicosanoids are involved in modulating the intensity and duration of inflammatory responses [ 4748 ], have cell- and stimulus-specific sources and frequently have opposing effects.
Thus, the overall physiological or pathophysiological outcome will depend upon the cells present, the nature of the stimulus, the timing of eicosanoid generation, the concentrations of different eicosanoids generated and the sensitivity of target cells and tissues to the eicosanoids generated.
Because of the relatively high amount of arachidonic acid in membrane phospholipids of cells involved in inflammation, this fatty acid is typically the major precursor for eicosanoid mediators, which are produced in greatly increased amounts upon cellular stimulation.
Thus, amongst the mix of eicosanoids produced, those synthesized from arachidonic acid e. In general arachidonic acid-derived eicosanoids act in a pro-inflammatory way, although this is an over-simplification since it is now recognised that PGE2, for example, has both pro- and anti-inflammatory effects, and that another eicosanoid derived from arachidonic acid, lipoxin A4, is anti-inflammatory [ 49505152 ]. Figure 2 Outline of the pathway of eicosanoid biosynthesis from arachidonic acid.
Fatty Acid Modification of Eicosanoid Profiles Animal studies have shown a direct relationship between arachidonic acid content of inflammatory cell phospholipids and ability of those cells to produce PGE2 [ 53 ], such that PGE2 production is increased by arachidonic acid feeding [ 53 ] and decreased by EPA or DHA feeding [ 535455 ]. It is well documented that PGE2 and 4 series-LT production by human inflammatory cells can be significantly decreased by fish oil supplementation of the diet for a period of weeks to months [ 141516185657 ].
EPA is also a substrate for the cyclooxygenase and lipoxygenase enzymes that produce eicosanoids, but the mediators produced have a different structure from the arachidonic acid-derived mediators, and this influences their potency.
Omega-3 Fatty Acids and Inflammatory Processes
Increased generation of 5-series LTs has been demonstrated using macrophages from fish oil-fed mice [ 55 ] and neutrophils from humans supplemented with oral fish oil for several weeks [ 141516 ]. Journal of the American Heart Association. But recently, fish oil supplements suffered a black eye.
An analysis of 18 randomized controlled trials published in leading journals between and found that only two out of the 18 had results that showed fish oil supplements compared to placebo offered benefits to people at high risk of cardiovascular events. Still, information from the NIH states that fish oil lowers high triglycerides an important measure of heart healthand it also seems to help prevent heart disease and stroke when taken in the recommended amounts.
Be aware that taking too much fish oil can actually increase the risk of stroke. Aging brings a greater risk for not only joint pain, but also cognitive impairment. The role of omega-3s for cognitive health is not as clear-cut as it is in heart health, but still bears consideration.
17 Science-Based Benefits of Omega-3 Fatty Acids
And a study, published in the British Journal of Nutrition infound that taking fish oil supplements reduced mental fatigue and increased reaction times in participants ages 18 to 35 years old. Although arthritis and diabetes are not directly related, they often coexist.
In fact, the Centers for Disease Control and Prevention, or CDC, found that more than half of people with diabetes also have arthritis. Again, omega-3s may be able to help, according to two reports. Typically, inflammation is meant to be transient, but under some circumstances the acute response can become chronic 3. Excess chronic inflammation is an important etiologic factor in a wide range of common chronic diseases, including cardiovascular disease 4diabetes 4Alzheimer and other neurologic diseases 5and cancer 6.
Numerous epidemiologic studies have reported associations between one or more of these biomarkers and the risk of various chronic diseases.
However, there is no consensus regarding which inflammatory biomarker is best. Instead, it appears that many researchers measure multiple biomarkers in any given study to increase the odds that associations with clinical outcomes will emerge.
Importantly, recent reports provide support for the idea that different diseases are associated with specific inflammatory biomarker profiles, which relates to dysregulation of specific immune cell populations 89. In the future one hopes that disease-specific inflammation biomarkers will be clearly defined.
In the meantime, readers interested in gaining a better understanding of the many issues surrounding biomarker selection are encouraged to read the report of the European branch of the International Life Sciences Institute, which commissioned a review of the biomarkers for monitoring inflammation in human nutritional studies There exists a large body of evidence suggesting that a variety of dietary factors can enhance or diminish inflammation The focus of this article is to describe how dietary fats affect inflammation and why it is an important human health consideration.
Current dietary guidelines for fats provide information about both the amount as well as the types of fats that should be consumed Evidence suggests that, in addition to the amount of fat, the types of fats consumed can have a major impact on human health. Their impact on the risk of cardiovascular disease has dominated the rationale for these recommendations for the past 50 y 14 — There is a growing recognition by leaders in the nutrition and health field that dietary fats can affect host inflammatory responses After reviewing the evidence, it seems reasonable that the impact of dietary fats on inflammatory status be factored into future dietary guidelines for these nutrients.
Current Status of Knowledge It appears that one way in which dietary fat is linked to inflammation is by promoting the translocation of microbial products from the gut into the bloodstream.
LPS is a very potent stimulus of inflammatory responses, with bioactivity in the microgram per liter concentration range. Importantly, there exists considerable diversity in the structure and bioactivity of LPS from microbial species This diversity suggests that individual gut microbiomes may be more or less proinflammatory on the basis of how effectively innate immune receptors recognize these microbially derived agonists.
Researchers have known for decades that gut microbes could be a source of systemic bacterial infection leading to sepsis and organ failure under a variety of medical circumstances Yet, it was only recently that researchers reported that dietary fat could promote endotoxin absorption.
The data suggest that high-fat feeding results in a chronic elevation in circulating endotoxin throughout the day and night. The authors reported that the high-fat diet altered the distribution and numbers of some of the microbial populations found in the gut. Interestingly, the authors went on to demonstrate that high-fat feeding affected a number of metabolic processes associated with metabolic syndrome e.
These responses were surprisingly similar in mice infused with LPS compared with those fed the high-fat diet. However, it was the authors' use of mice carrying a deletion of CD14, a critical component of the LPS receptor, which provided the most compelling evidence that many of the adverse effects of high-fat feeding may be a consequence of activation of inflammatory signaling pathways.
Current thinking is that the acute postprandial inflammatory response associated with fat consumption is mediated by endotoxin, primarily derived from gut microflora Others suggested, however, that many foods contain endotoxin or related proinflammatory compounds that, upon absorption, directly stimulate inflammatory responses Those foods with the most in vitro inflammatory activity included meats, cheeses, and dairy products.
Regardless of source, once absorbed, endotoxin is shuttled between chylomicrons and HDL particles via a specific binding proteins and soluble receptors present in the circulation There is a strong correlation between postprandial lipemia and net endotoxin absorption. Evidence suggests that chylomicrons play a critical role in the absorption and transport of endotoxin.
Factors that promoted fat absorption, such as emulsification, also enhanced endotoxin absorption. Recently, Mani et al. After overnight feed deprivation, pigs were fed a meal containing The meal was consumed within 10 min, then blood samples were taken hourly for 5 h. Pigs fed coconut oil, rich in SFAs, had the highest circulating concentrations of endotoxin followed by those that were fed vegetable oil and then those fed fish oil.
Additional testing on freshly isolated samples of ileum showed that the fats had not affected overall intestinal integrity or permeability. The authors suggested that the endotoxin absorbed was most likely transported by way of lipid raft—mediated endocytosis.