Omega-3 fatty acids, and in particular eicosapentaenoic fatty acid (EPA), have been the subject of increasing interest in scientific research due to their potential effects as anti-inflammatory agents.
In this article, we will review the accumulated scientific evidence on the benefits of EPAs in reducing inflammation and its applicability in clinical settings, such as supplement-based interventions.
We hope you can enjoy this interesting article.

Inflammation

Inflammation is a fundamental biological response that the body uses to defend itself against injury and disease.
However, chronic inflammation has been associated with a number of diseases such as cardiovascular diseases, type II diabetes, and autoimmune disorders.

The inflammatory process aims at the destruction of pathogens and subsequent tissue repair helps restore homeostasis in affected or damaged sites.
Typically, in acute inflammation, there is initial redness, swelling, warmth, pain, and loss of function, and involves interactions between many cell types, producing and responding to a number of chemical mediators.

When an inflammatory response occurs, it is normally regulated in such a way that it does not cause excessive harm to the host, is self-limiting, and resolves quickly.
This self-regulation involves the activation of negative feedback mechanisms such as the secretion of anti-inflammatory mediators, the inhibition of pro-inflammatory signaling cascades, the elimination of inflammatory mediator receptors, and the activation of regulatory cells.
https://doi.org/10.1007/s11515-011-1123-9

When these mechanisms are properly controlled, regulated inflammatory responses are essential to maintain homeostasis.
Pathological inflammation involves a loss of tolerance and/or regulatory processes.
When it becomes excessive, irreparable damage to host tissues and disease can occur.
Regardless of the cause of inflammation, the response involves four main events:

• · An increased blood supply to the site of inflammation.
• · Increased capillary permeability caused by the retraction of endothelial cells.
  This allows larger molecules, which are not normally able to pass through the endothelium, to do so and thus supply soluble mediators to the site of inflammation.
• · Migration of leukocytes from capillaries to surrounding tissue.
  This is aided by the release of chemotactics from the site of inflammation and by the upregulation of adhesion molecules in the endothelium.
  Once in the tissue, the leukocytes travel to the site of inflammation.
• · Release of leukocyte mediators at the site of inflammation.
  These may include mediators such as prostaglandins, leukotrienes, cytokines, reactive oxygen species, histamine, and enzymes such as matrix proteases.
  The substance released will depend on the type of cell involved, the nature of the inflammatory stimulus, the anatomical site involved, and the stage during the inflammatory response.

The mediators listed above play a role in host advocacy as a general rule, but when they occur inappropriately or unregulated, they can cause damage to host tissues and lead to disease, especially chronic disease.

Several of these mediators can come together to amplify the inflammatory process by acting, for example, as chemotactics.
Some of the inflammatory mediators can escape from the inflammatory site into the circulation and from there exert systemic effects.
For example, the cytokine interleukin (IL)-6 induces hepatic synthesis of acute-phase C-reactive protein, while the cytokine tumor necrosis factor (TNF)-α causes metabolic effects in skeletal muscle, adipose tissue, and bone.
DOI:10.1017/S0007114509377867

Digging deeper into fatty acids

Generally, omega-6 fatty acids (e.g., arachidonic acid) promote inflammation, while omega-3 fatty acids (such as eicosapentaenoic acid and docosahexaenoic acid) have anti-inflammatory properties.
Omega-3 fatty acids buffer inflammation through multiple pathways.

If you want to read about omega-3 fatty acids in detail, we recommend you click here, and you can read a little more in one of our previous posts.

On the one hand, omega-3 fatty acids inhibit the formation of pro-inflammatory eicosanoids derived from omega-6 fatty acids such as prostaglandin E2 and leukotriene B4, and on the other hand, these fatty acids can form several potent anti-inflammatory lipid mediators called resolvins and protectins.
These substances, acting together, directly or indirectly suppress the activity of nuclear transcription factors, such as NFκB, and reduce the production of pro-inflammatory enzymes and cytokines, including COX-2, tumor necrosis factor (TNF)-α, and interleukin (IL)-1β.

Accumulating evidence supports the use of EPA Omega-3s as adjuvants in the treatment of chronic inflammatory diseases.
It has been observed that supplementation with these polyunsaturated fatty acids can reduce the levels of inflammatory markers in patients with rheumatoid arthritis, Crohn’s disease, and other autoimmune diseases.
In addition, it has been shown that omega-3s may have a beneficial role in preventing cardiovascular disease by reducing vascular inflammation. https://doi.org/10.1016/j.ejphar.2015.08.050

Influence of polyunsaturated fatty acids on inflammatory cells

Polyunsaturated fatty acids (PUFAs) can influence the function of inflammatory cells and, therefore, inflammatory processes, through various mechanisms.

Non-esterified PUFAs can act directly on inflammatory cells through surface or intracellular fatty acid receptors; the latter may include transcription factors such as peroxisome proliferator-activated receptors (PPARs).

In addition, they can be oxidized – enzymatically or not enzymatically – and oxidized derivatives can act directly on inflammatory cells through surface or intracellular receptors; oxidation can occur in the esterified or non-esterified form into more complex lipids, including circulating or cell membrane phospholipids and intact lipoproteins such as low-density lipoproteins (LDL).

PUFAs can be incorporated into the phospholipids of inflammatory cell membranes (as described above).
Here they play important roles by ensuring the correct environment for membrane protein function, maintaining membrane fluidity, and influencing the formation of lipid rafts. https://doi.org/10.1146/annurev-nutr-080508-141205

Membrane phospholipids are substrates for the generation of second messengers such as diacylglycerol and it has been shown that the fatty acid composition of these second messengers, which is determined by that of the precursor phospholipid, can influence their activity.

In addition, membrane phospholipids are substrates for the intracellular release of non-esterified PUFAs.
These, when released, can act as signaling molecules, ligands (or ligand precursors) for transcription factors, or precursors for the biosynthesis of lipid mediators involved in regulating many cellular and tissue responses, including aspects of inflammation and immunity.

Active ω3 immunity

The supplement developed by Salengei, Active Ω3 Immunity, comes in the form of pearls and offers a valuable option for those who want to take advantage of the benefits of omega-3 fatty acids conveniently and effectively.
By promoting a balance in the body’s inflammatory response, they are a valuable nutritional intervention that would serve as a preventive measure in cases of chronic inflammation.

By inhibiting the formation of pro-inflammatory eicosanoids and promoting anti-inflammatory lipid mediators, Active Ω3 Immunity beads may contribute to the regulation of key factors in the immune response, which can potentially have a positive impact on overall health.

Conclusion

Omega-3s, and especially EPAs, through their ability to modulate inflammation, have shown promise as anti-inflammatory agents in a variety of clinical conditions.
However, more research is needed to fully understand its mechanisms of action and optimize its clinical use.

Meanwhile, supplementation with Active Ω3Immunity , as part of a comprehensive treatment strategy, could be a valuable and safe option for patients with chronic inflammatory diseases and inflammation-related disorders.