Omega- for inflammation -
In one small study, very low daily doses of fish oil led to complete remission in 10 lupus patients. In a different twist, researchers studying the blood of people with lupus found far lower levels of omega-3 fats compared to their healthy counterparts. In similar studies, lupus patients had lower levels of omega-3 fats than people with heart disease did.
Other Conditions Heart Health. Omega-3s have had their ups and downs relative to heart health, hailed as a cardiac miracle at one point and a disappointment at others.
They concluded that fish oil supplements significantly lowered the risk of most heart-related conditions, including heart attack, coronary heart disease CHD and cardiovascular disease CVD as well as CHD- and CVD-related death. The amount of omega-3s varied among trials, from mg to 4, mg a day.
Higher doses were associated with better outcomes. These findings were reinforced by a large study involving nearly half a million people who were followed for eight or nine years. It, too, found that regular use of fish oil supplements led to lower rates of cardiovascular disease, heart attack and death.
Fish oil was even more protective for people with high blood pressure. Whether fish oil benefits heart health remains controversial. And a analysis of seven clinical trials found higher doses of fish oil might increase the risk of atrial fibrillation or irregular heartbeat.
So the debate continues. Cognitive Health. Aging brings a greater risk of cognitive impairment. This may be due to difficulty converting DHA from supplements into forms that can cross easily into the brain. Although arthritis and diabetes are not directly related, they often coexist.
The Centers for Disease Control and Prevention CDC found that more than half of people with diabetes also have arthritis. Some older research reported that omega-3s might be able to stave off type 1 diabetes if given early enough to infants and young children.
And one of the largest and most recent adult trials to date — a prospective, observational study of nearly , people in the U. Food vs. The U. Department of Agriculture recommends at least two servings a week 3. There are some problems with sourcing omega-3s from food, though. For instance, not everyone likes, has access to or can afford fresh or frozen fish, especially wild-caught salmon, which is particularly high in omega-3s.
In these cases, supplements are an important option. Vegetarian and Vegan Sources Vegetarians and vegans — a growing portion of the population — are often left out of omega-3 discussions.
Some plant foods, including Brussels sprouts, kale, spinach, flaxseeds, chia seeds and walnuts, contain alpha-linolenic acid.
In addition, intraperitoneal injection of RvE1 with LXA 4 decreased microgliosis and astrogliosis in the cortex and hippocampus of AD mice One in vivo study proposed two different mechanisms of actions for RvEs using a model of LPS-induced depression in mice.
Firstly, intracranial injection of RvE1 and RvE2 produced anti-depressant effects similar to those observed by activating ChemR23, a G-coupled receptor activated by chemerin 62 and RvE1 63 , suggesting the involvement of this receptor in depression.
Secondly, inhibition of the mTORC1 pathway was able to prevent the anti-depressant effects of RvE1 In an in vivo transgenic mouse model of AD, RvE1 was shown to exert its effects through down-regulation of various pro-inflammatory factors. Specifically, peripheral RvE1 injection reduced levels of IL-6, IL-1β, IL, granulocyte-macrophage colony-stimulating factor GM-CSF , IFN-γ, TNF-α, monocyte chemoattractant protein 1 MCP-1 , macrophage inflammatory protein MIP -1a, and MIP1b in the prefrontal cortex The evidence summarized in this section supports the potential of RvEs, similar to RvDs, to alleviate depression-like behavior, which would occur via mTORC1 activation.
In terms of neurodegenerative disorders, studies clearly present RvEs as beneficial agents against the increased levels of cytokines and pro-inflammatory factors present in those conditions.
Behavioral effects of PD1 administration were measured in three in vivo studies, one in the context of epilepsy and two in the context of stroke, both conditions which are associated with increased central inflammation affecting neurogenesis-related cognitive processes.
Intracranial PD1 administration improved cognitive function, specifically non-spatial recognition memory, in the novel object recognition task in kainic acid-induced epilepsy in mice PD1 also reduced frequency and seizure duration and prevented weight loss Additionally, intravenous injection of PD1 and its aspirin-triggered isomer AT-PD1 improved neurological recovery in rat models of ischemic stroke using middle cerebral artery occlusion 51 , Cellular outcomes were investigated in nine studies both in vivo and in vitro , predominantly using models of AD and ischemia.
Intravenous administration of PD1 in vivo reduced immunoglobulin G IgG immunoreactivity in the cortex, subcortex, and whole right hemisphere of rats subject to ischemic stroke It also inhibited astrocyte and microglia activation in the penumbra of ischemic rats Likewise, intracranial infusion of PD1 in epileptic mice decreased astrogliosis and microgliosis in the hippocampus, and increased neuroblasts migration in the hilus In a mouse model of TBI, intracranial administration of PD1 also improved parenchymal cell survival In vitro , PD1 treatment decreased Aβ 42 production 56 and prevented Aβ 42 -induced apoptosis and increased cell viability in two human models of AD, both using cortical neuron-glia co-culture 32 , This was also observed upon treatment with protectin isomer, PDX, in a human bone-marrow derived neuroblastoma cell model of AD In a rat dopaminergic mesencephalon neurons model of PD, PD1 treatment decreased dendritic retraction and increased neuronal survival Finally, in an in vitro model of ischemia, PDX also increased proliferation of mice subventricular zone neural progenitors One in vivo and two in vitro studies investigated the mechanisms of PD1.
In vivo , transcription and expression of IL-1β and TNF-α were reduced in the hippocampus upon PD1 intracranial administration in a murine model of epilepsy In an in vitro model of AD, PD1 administration reduced Aβ 42 production through repression of pro-inflammatory molecules, including COX-2 and TNF-α Furthermore, PD1 enhanced expression of anti-apoptotic proteins of the B-cell lymphoma 2 Bcl-2 gene family 32 and reduced caspase-3 activity in cortical human neuronal cells in vitro Based on the evidence summarized in this section, protectins are especially useful in reducing behavioral deficits observed in neurological disorders, most likely via reducing microgliosis and pro-inflammatory cytokines levels.
One in vivo study investigated the behavioral effects of treatment with MaR1, whereas three in vitro studies assessed cellular outcomes. In an in vivo mouse model of stroke, intracranial administration of MaR1 reduced neurological impairments over time On a cellular level, administration of MaR1 protected against brain cell death and inhibited the degradation of postsynaptic density protein 95 PSD95 and synapsin.
Furthermore, MaR1 administration also inhibited neutrophil infiltration and glial activation in the cortex In vitro , MaR1 treatment prevented cell death in human bone-marrow derived neuroblastoma cell models of ALS and AD 46 , MaR1 also stimulated an increase of Aβ 42 phagocytosis in embryonic human microglial cells All three studies previously mentioned investigated the mechanisms of action of PD1.
In an in vivo mouse model of stroke, expression of TNF-α, IL-1β, and MCP-1 in the cortex was reduced by intracranial administration of MaR1. Furthermore, MaR1 decreased NF-κB activation through down-regulation of p65 phosphorylation Similar effects were seen in vitro , with MaR1 treatment decreasing levels of phosphorylated NF-κB in human bone-marrow derived neuroblastoma cells MaR1 treatment of embryonic human microglia also induced a reduction in pro-inflammatory markers including CD11b, major histocompatibility complex class II MHC-II , CD86, CD40, and CD33 The limited evidence available on maresins suggests that they might benefit neurological conditions, specifically by reducing cell death and inflammatory factors, which may be related to decreased NF-κB pathway activation.
This review summarizes evidence on the beneficial effects of resolvins, protectins and maresins, in the treatment of psychiatric, neurodegenerative, and neurological disorders Figure 2.
Overall, treatment with both RvD and RvE improved depressive-like behaviors in various animal models of depression, whereas PD1 and MaR1 ameliorated neurological function. On a cellular level, RvD1 and RvD2 increased serotonin levels in a model of depression, and decreased gliosis in neurodegenerative disorders.
In contrast, PD1 and PDX prevented neurite and dendrite retraction and apoptosis in models of neurodegeneration, while MaR1 reduced cell death across all studies.
In terms of mechanisms, all SPMs down-regulated pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α. These findings suggest that not only do SPMs have anti-inflammatory properties across different models, but also possess characteristic therapeutic effects depending on the condition.
Figure 2. Comparison of behavioral, cellular, and molecular findings upon treatment with SPMs in the context of psychiatric, neurodegenerative, and neurological disorders. Despite the scarce number of studies conducted in psychiatric disorders, differences among specific SPMs could be drawn on several levels.
In particular, RvD1 and RvEs were the most effective in improving depressive symptoms across several mouse models 36 , 39 , 48 , This could be explained by their mechanistic actions, which were notably distinct between psychiatric and neurological conditions.
The mTORC1 pathway, which is a key signaling pathway in the effectiveness of antidepressants 64 , was found to underlie the behavioral effects of resolvins 36 , Moreover, all of these are key elements involved in neurogenesis 66 , which is impaired by pro-inflammatory cytokines 67 and has been shown to be rescued by n-3 PUFAs treatment after IL-1β challenge in vitro With respect to neurodegenerative disorders, none of the SPMs could be distinguished in terms of better therapeutic effects.
While apoptosis or gliosis were equally reduced by RvD1, RvE1, PD1, and MaR1 in in vivo and in vitro models, the benefits observed in ex vivo studies using patient-derived cells remained on a trend level 41 or were restricted to specific sub-groups Although it is difficult to disentangle the underlying cause of these seemingly puzzling findings, the situation can be closely related to the reality of research into AD therapy.
Many anti-inflammatory drugs appear promising at pre-clinical stages but are not effective in clinical trials, presumably due to the complexity of the disorder and the number of interacting factors Further investigation is thus necessary to achieve a clearer understanding of SPMs in neurodegenerative disorders.
Although, maresins and protectins have not been examined in the context of depression, the evidence was conclusive in neurological disorders, where they appear to have a greater potential. PD1, PDX, and MaR1 improved neurological function in animal models of ischaemia, and TBI 51 , 53 , In line with this, PD1 limited cell death, highlighting its neuroprotective abilities.
MaR1 likely had a greater effect in these conditions due to its presence in macrophages and its more potent role in dampening the activation of microglia 69 , which are more acutely and severely triggered in those conditions.
Additionally, MaR1 promotes tissue regeneration, which could be of increased therapeutic value in ischemic stroke Thus, the ability of specific metabolites to improve behavioral, cellular and mechanistic components differentially in psychiatric and neurodegenerative disorders could be a basis for new personalized therapeutic strategies.
Although current pharmacotherapies for AD and PD appear to slow the progression of cognitive impairment, the benefits have often found to be marginal and non-sustained Additionally, up to one third of MDD patients fail to respond to first-line pharmacological treatment 71 , which has been associated with elevated plasma pro-inflammatory factors expression N-3 PUFAs have been approved as safe when administered in doses up to 3 g per day and minor side-effects are rare Recent reviews and meta-analysis have reported a clinical efficacy of n-3 PUFAs treatment, which might be partly attributable to SPMs, in MDD and AD patients 76 , More interestingly, the majority of the animal studies so far only used males, which have recently been shown to have higher baseline levels of n-3 PUFAs metabolites than females in brain tissue The single study using female mice reported positive effects of RvE1 on inflammatory factors, however, this does not allow for direct comparison between sexes With women being at increased risk of developing MDD and AD 79 , 80 , further insight into this question is necessary as they might even more particularly benefit from this type of intervention.
Based on the findings from our review, personalized SPMs treatment could be a therapeutic possibility. RvD1, RvD2, or RvE1 could prove to be beneficial in psychiatric conditions, like depression, while MaR1 or PD1 would be optimally targeted toward neurological conditions.
Although more studies are required to determine their exact influence and production in the brain, our review indicates a potential promising approach for tailored therapy with SPMs. With further research, this could lead to subsequent dietary recommendations and nutritional interventions in the treatment of psychiatric, neurodegenerative or neurological conditions, as n-3 PUFAs have been demonstrated to raise specific SPMs levels This review has few limitations that must be considered, such as the number of studies meeting the inclusion criteria and the prominence of cognitive and neurological compared with psychiatric studies.
Additionally, dosage and route of administration between metabolites was also variable. Nonetheless, this is the first review to compare the effects of SPMs in the context of psychiatric, neurodegenerative and neurological disorders and sheds light on the differential mechanisms mediating their beneficial properties.
Further research is needed to elucidate the exact mechanisms of action of these metabolites, as well as the extent of their anti-inflammatory properties, in order to discern which disorder they should optimally target.
All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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The data arose from blood testing inflqmmation in and at a now defunct Omega- for inflammation as part of routine clinical assessments. The study inflam,ation data from more Body Weight Classification 44, blood Niflammation. The samples were stratified via their Omega-3 Index, a measurement pioneered by one of authors, William Harris, PhD. Harris, who founded the testing firm OmegaQuant Analytics, is now the head of the Fatty Acid Research Institute. His coauthors, Michael McBurney, PhD, and Nathan Tintle, PhD, are also members of the institute as well has having other academic affiliations, as does Harris. Fog fatty acids have been linked fog Omega- for inflammation health benefits. In particular, they Inflammatiob help promote brain and inflammztion health, reduce inflammation, and protect against Fleet Fuel Tracking chronic conditions. Depression is one of the most imflammation mental disorders in the world 1. Symptoms often include sadness, lethargy, and a general loss of interest in life 2. Anxietyanother common disorder, is characterized by feelings of fear, panic, and restlessness 3. Interestingly, studies indicate that people who consume omega-3s regularly are less likely to have depression 45. There are three types of omega-3 fatty acids: alpha-linolenic acid ALAeicosapentaenoic acid EPAand docosahexaenoic acid DHA.
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